1) All of The Following Can Cause Polyuria, Except:: Description
1) All of The Following Can Cause Polyuria, Except:: Description
1) All of The Following Can Cause Polyuria, Except:: Description
Answer: C* Hypothyroidism
Description:
Polyuria is increased urine output to more than 3 liters per day.
In hyperglycemia; osmotic pressure of presence of glucose in renal tubules pulls more water
and increase the urine output.
In case of DI; impaired secretion or unresponsiveness to ADH lead to diuresis and increased
hypo-osmolar urine leading to polyuria
In psychogenic cases; increased amount of fluid intake (psychogenic polydipsia) lead to
increase water excretion and polyuria
In case of hypercalcemia: The high tubular concentration of calcium makes the net charge of
the tubular fluid more positive. This tends to inhibit the back-leak of K+ ions, This tends to
inhibit the back-leak of K+ ions, since they are also positively charged, and 'like' charges
repel. Again, this inhibits the above pump, resulting in more Na+, and thus more water, in the
lumen leading to polyuria.
Answer: D* Hyperkalemia
Description:
Hypokalemia not hyperkalemia is a cause of polyuria.
In thick ascending lobe of Henle, there is a pump which excrete potassium ions into the lumen
and reabsorb sodium back instead. In case of hypokalemia sodium reabsorption will be
decreased leading to less water reabsorption and increased urine volume.
Other mentioned causes are known to cause polyuria.
Description:
Hypokalemia not hyperkalemia is a cause of polyuria.
In thick ascending lobe of Henle, there is a pump which excrete potassium ions into the lumen
and reabsorb sodium back instead. In case of hypokalemia sodium reabsorption will be
decreased leading to less water reabsorption and increased urine volume.
Other mentioned causes are known to cause polyuria.
Urine
4) All of the following can cause hematuria, except:
A. Renal stone
B. Renal tuberculosis
C. Malignant hypertension
D. Renal tubular acidosis
E. Cystitis
Description:
RTA is a disorder causing Increased acidity of blood due to impaired renal ability to maintain
acid-base balance, and it is not a cause of hematuria.
Causes of hematuria are mentioned below:
- Infection (pyelonephritis, cystitis, UTI, urethritis, endocarditis…)
- Stone in renal tract
- Cancers of any part of renal system
- Renal epithelial Injury
- Glomerulonephritis, IgA nephropathy, nephritic syndrome
- Blood disorders
- Drugs: cyclophosphamide ; hemorrhagic cystitis
- Papillary necrosis
- Accelerated HTN
- Renal cyst
Answer: D* Pregnancy
Description:
In pregnancy; presence of glucosuria and trace proteinuria considered normal due to
physiological increase in GFR.
Causes of hematuria are mentioned below:
- Infection (pyelonephritis, cystitis, UTI, urethritis, endocarditis…)
- Stone in renal tract
- Cancers of any part of renal system
- Renal epithelial Injury
- Glomerulonephritis, IgA nephropathy, nephritic syndrome
- Blood disorders
- Drugs: cyclophosphamide ; hemorrhagic cystitis
- Papillary necrosis
- Accelerated HTN
- Renal cyst
Answer: D* Amyloidosis
Description:
Causes of hematuria are mentioned below:
- Infection (pyelonephritis, cystitis, UTI, urethritis, endocarditis…)
- Stone in renal tract
- Cancers of any part of renal system
- Renal epithelial Injury
- Glomerulonephritis, IgA nephropathy, nephritic syndrome
- Blood disorders
- Drugs: cyclophosphamide ; hemorrhagic cystitis
- Papillary necrosis
- Accelerated HTN
- Renal cyst
Description:
Cold exposure is not known to cause hematuria
Causes of hematuria are mentioned below:
- Infection (pyelonephritis, cystitis, UTI, urethritis, endocarditis…)
- Stone in renal tract
- Cancers of any part of renal system
- Renal epithelial Injury
- Glomerulonephritis, IgA nephropathy, nephritic syndrome
- Blood disorders
- Drugs: cyclophosphamide ; hemorrhagic cystitis
- Papillary necrosis
- Accelerated HTN
- Renal cyst
Description:
The most worrisome causes of painless hematuria is renal and bladder cancers.
Renal cell carcinoma may stay symptomless for later stage but it may present with triad of
hematuria, flank pain and flank mass.
80-90% of bladder cancer cases are present with painless hematuria.
Other mentioned cases presents with pain.
9) All of the following can cause proteinuria in excess of 3 grams per 24 hours, except:
A. Membranous glomerulonephritis
B. Malignant hypertension
C. Diabetic nephropathy
D. Obstructive uropathy
E. Renal amyloidosis
Description:
Heavy proteinuria is caused by glomerular damage, while tubular damage can cause less than
1g/ day proteinuria.
All mentioned choices are a cause of glomerular damage and can cause heavy proteinuria, but
obstructive uropathy will lead to interruption of urine output and may cause anuria and post
renal acute renal failure.
10) The protein present in the greatest quantity in the urine of normal people is:
A. Albumin
B. Tamm-Horsfall protein
C. Gamma globulin
D. Amylase
E. Bence-Jones protein
Description;
It is normal to excrete tiny amount of protein (known as Tamm-Horsfall protein) and it
present in normal people.
Other types of protein should not be present in urine and if present in significant amount so it
indicates further evaluation.
11) All of the following statements are correct about routine urine examination, except:
A. Specific gravity of 1015 is normal
B. Red blood cell cast is normal finding
C. One red blood cell is normal finding
D. One white blood cell is normal finding
E. Negative sugar is normal finding
Description:
In urinalysis; the presence of RBC’s casts indicates nephritic syndrome and never be normal.
Here is a quick explanation about urinalysis:
Urinalysis: It has 2 parts (dipstick and microscopic analysis)
- Color normally yellow, darker if dehydrated and white if well hydrated, also can
be red if RBC's, myoglobin or Hb present, can be turbid or green if infection
- Volume normally 0.5 ml/kg/hr
o Anuria: if less than 100ml/day
o Oliguria: if less than 300ml/day
o Polyuria: if > 3 liters/day
- Specific gravity normally 1.002 to 1.025
o High in dehydration, DM,
o Low in DI, chronic renal failure
- PH normally PH: 6
o Alkaline in proteus infection
o If early morning urine is alkaline: Distal RTA should be suspected
- Urine glucose: usually indicates DM but it is false positive in pregnancy, vitamin C
intake, tetracycline or levodopa use
- Ketones can present in DKA or due to starvation
- Urine protein can cause frothy looking urine, normally < 50 mg/day
- Microscopy:
o WBC > 10 hpf indicates UTI, WBC's casts found in acute pyelonephritis
o Persistent WBC's in urine with negative Culture can be TB.
o RBC's > 5 hpf indicate hematuria, RBC's Casts: found in glomerulonephritis
o Crystals
Urinary Tract Infections.
12) The commonest cause of urinary tract infection is:
A. Proteus species
B. Escherichia coli
C. Klebsiella
D. Pseudomonas
E. Citrobacter species
Description:
E. coli is the most common bacteria that cause UTI, this is related to the fact that these
bacteria live in GI tract and get entered to urethra when fecal contamination occur.
13) The most definitive diagnosis for urinary tract infection is:
A. Presence of 10 000 bacteria per ml in urine culture
B. Presence of WBC in the urine
C. Presence of WBC and protein in the urine
D. Presence of 100 000 bacteria per ml in a properly collected urine by culture
E. Presence of pain in the right loin
Answer: D* Presence of 100 000 bacteria per ml in a properly collected urine by culture
Description:
The most accurate test to confirm the diagnosis of UTI is urine culture, presence of 100,000
colony forming units per ml in culture will be diagnostic.
WBC’s in urine, symptoms of UTI are diagnostic but culture still the most accurate test.
14) Regarding urinary tract infection all of the following are true, except:
A. Frequency and foul smelling urine are presenting complaints
B. First morning specimen voided is not suitable for colony count
C. Fever
D. Abdominal pain
E. Nearly always causes pyuria
Answer: B* First morning specimen voided is not suitable for colony count
Description:
A midstream urine specimen at anytime can be used for colony count and for any test to
diagnose UTI
Fever abdominal pain, dysuria, frequency and foul smelling urine may be a features or
presenting complains
Description:
Recurrent UTI may be a cause of chronic renal impairment due to ascending transmission of
infection to kidneys which interfere with normal kidney function.
In case of recurrent UTI, children may be affected due to congenital anomalies of urinary
tract.
The most common bacteria in recurrent UTI is E. coli
Females have shorter urethra than males so it is more easy to transmit bacteria into urinary
tract and then UTI will be more common in females.
The aim of management in UTI is clinical cure and no need for treatment of asymptomatic
bacteruria in non-pregnant patients, but here in recurrent UTI the aim is to identify the cause
of recurrence and prevent renal damage and impairment.
Glomerulonephritis.
16) Which of the following urinary findings is most characteristic of glomerulonephritis:
A. Hyaline cast
B. Granular cast
C. RBCs cast
D. WBCs cast
E. Epithelial cast
Description:
RBC’s casts are a RBC’s stick together that pass through the glomerulus in case of nephritic
syndrome.
WBC’s cast if present indicates pyelonephritis
Hyaline casts may present with Glomerulonephritis, pyelonephritis, CKD or congestive heart
failure.
Granular casts are indicative of UTI, urinary stasis or strenuous exercise
Epithelial cell casts indicate tubular damage.
Description:
Erythrocyte casts (or also known as RBC’s casts) are the main feature of nephritic syndrome
(as a part of glomerulonephritis).
Hyaline casts may present with Glomerulonephritis, pyelonephritis, CKD or congestive heart
failure.
Granular casts are indicative of UTI, urinary stasis or strenuous exercise
Proteinuria and hematuria also present in glomerulonephritis but the presence of RBC’s cast
is the most specific finding over all other choices.
18) Acute glomerulonephritis may be associated with which one of the following:
A. Glycosuria
B. Elevated serum cholesterol
C. Elevated serum complement
D. Encephalopathy
E. Hypercalcemia
Description:
Complement level will be low in most cases of glomerulonephritis.
In acute glomerulonephritis the glomerulus will be destructed and allow the passage of large
molecules into the urine (like proteins, RBC’s and glucose…) so glycosuria occur.
Liver will increase its work to compensate for protein loss, so overproduction of cholesterol y
liver may occur leading to hypercholesterolemia.
Encephalopathy occur due to increased blood pressure resulting from activation of RAAS.
Hypercalcemia is not uncommon in case of acute glomerulonephritis and acute renal
impairment.
19) Complications of post streptococcal acute glomerulonephritis may include all of the
following, except:
A. Hyperkalemia
B. Hypernatremia
C. Encephalopathy
D. Pulmonary edema
E. Anuria
Answer: B* Hypernatremia
Description:
Hyperkalemia, hyponatremia and hypocalcemia will occur in glomerulonephritis.
Hyponatremia here is dilutional and may respond to diuretics.
Encephalopathy occur due to HTN and treated as hypertensive encephalopathy
Oliguria or anuria may be present indicating renal shutdown.
20) Which of the following is not associated with post streptococcal glomerulonephritis:
A. Hematuria
B. Fatty casts
C. Red blood cell casts
D. Edema
E. Oliguria
21) Manifestations of the nephritic syndrome include all of the following, except:
A. Oliguria
B. Hypertension
C. Pulmonary edema
D. Hematuria
E. Peripheral neuropathy
Description:
Peripheral neuropathy never be a symptoms of nephritic syndrome but hypernensive
encephalopathy may present.
In nephritic syndrome: an insult to the nephron cause it to pass high amount of protein in
urine but less than 3.5g/day as well as RBC’s and RBC casts.
HTN occur due to activation of Renin angiotensin system (RAAS) because of inflammatory
cells which infiltrate and decrease nephron perfusion leading to oliguria.
Pulmonary edema will manifest due to sodium water retention and decreased albumin level
along with increased hydrostatic blood pressure
22) In which of the following diseases would you expect to find the nephritic syndrome:
A. Pyelonephritis
B. Acute glomerulonephritis
C. Urinary tract infection
D. Mild hypertension
E. Amyloidosis
Description:
Acute glomerulonephritis present in either nephritic of nephrotic syndrome.
DM and hypertension are the most common causes of nephrotic range proteinuria
Amyloidosis is a well known cause of nephrotic syndrome
Chronic Pyelonephritis and vesicourethral reflux disease with recurrent UTI are known to
cause nephrotic syndrome.
Nephrotic Syndrome.
24) The nephrotic syndrome is characterized by all the following, except:
A. Edema
B. Proteinuria
C. Hypoalbuminemia
D. Hyperlipidemia
E. Hypertension
Answer: E* Hypertension
Description:
Nephrotic syndrome results from glomerular damage and heavy >3.5 g/day proteinuria occur
leading to hypoalbuminemia and generalized edema, and hypercholesterolemia due to liver
trying to compensate hypoalbuminemia.
Hypertension is not a feature of nephrotic syndrome but present in nephritic syndrome.
Answer: A* Hypocholesterolemia
Description:
Hypercholesterolemia in nephrotic syndrome results from increasing liver work to
compensate for hypoalbuminemia leading to produce more protein and more lipids.
Nephrotic syndrome results from glomerular damage and heavy >3.5 g/day proteinuria occur
leading to hypoalbuminemia and generalized edema, and hypercholesterolemia due to liver
trying to compensate hypoalbuminemia.
26) All of the following can cause calcification in the renal tract, except:
A. Schistosomiasis
B. Hyperparathyroidism
C. Tuberculosis
D. Nephrotic syndrome
E. Hydatid cyst
Description:
Normally tubule cells reabsorb water. In ATN the tubal cells are damaged urine can't be
concentrated urine osmolality is equal to blood osmolality (this is called Isosthenuria)
28) The following are recognized causes of acute renal failure, except:
A. Goodpasture’s syndrome
B. Hemolytic uremic syndrome
C. Minimal change disease
D. Scleroderma crisis
E. Post infectious glomerulonephritis
Description:
Minimal change disease is a disease of nephrotic syndrome, in which no acute renal
impairment occur.
Goodpasture’s syndrome is a vasculitis that affect lung and kidneys which may result in renal
impairment
Scleroderma crisis is a rare but life threatening complication of scleroderma characterized by
presence of severe hypertension accompanied with rapidly progressive renal impairment,
hypertensive encephalopathy, congestive heart failure with Microangiopathic hemolytic
anemia.
Hemolytic uremic (HUS): is a group of disease that include: Acute renal failure,
Microangiopathic haemolytic anemia MAHA and Thrombocytopenia
29) Causes of acute renal failure include all the following except:
A. Severe dehydration
B. Severe burn
C. Uncomplicated urinary tract infection UTI
D. Severe hemorrhage
E. Hemolytic uremic syndrome
Description:
Uncomplicated UTI is not likely to cause renal impairment but recurrent UTI may be a cause
Dehydration, burn and severe hemorrhage are all a cause of prerenal acute renal failure.
Hemolytic uremic (HUS): is a group of disease that include: Acute renal failure,
Microangiopathic haemolytic anemia MAHA and Thrombocytopenia
30) Complications of acute renal failure include each of the following, except:
A. Pulmonary edema
B. Hyperkalemia
C. Hypernatremia
D. Encephalopathy
E. Acidosis
Answer: C* Hypernatremia
Description:
In acute renal failure hyperkalemia, hyponatremia and hypocalcemia are the main electrolyte
disturbances to occur.
Pulmonary edema due to sodium water retention, encephalopathy occur due to hypertension
while wide anion gap metabolic acidosis occur due to accumulation of uric acid.
31) A patient with acute renal insufficiency is likely to develop any of the following
disturbances, except:
A. Hypoalbuminemia
B. Hyperkalemia
C. Hypocalcemia
D. Hypernatremia
E. Hyperphosphatemia
Answer: D* Hypernatremia
Description:
In acute renal failure hyperkalemia, hyponatremia and hypocalcemia are the main electrolyte
disturbances to occur.
Hyperphosphatemia and hypoalbuminemia are also a features.
Answer: D* Hypernatremia
33) One of the following is not an absolute indication for dialysis in chronic renal failure
patients:
A. Hyperkalemia
B. Hypercalcemia
C. Pulmonary edema
D. Metabolic acidosis
E. Pericarditis
Answer: B* Hypercalcemia
Description:
Hypercalcemia first line of treatment is I.V saline and diuretics.
Here is a list of indications for dialysis in renal impairment patients:
- Uremic symptoms (pericarditis, encephalitis, platelet dysfunction and bleeding,
convulsions)
- Fluid overload
- Refractory hyperkalemia >7meq/l
- Acidosis PH < 7.2
- Serum creatinine > 10 mg/dl
- Serum urea > 200 mg/dl
Answer: C* Diabetes
Description:
DM and HTN are the most common causes of end stage renal disease.
Nephropathy can be decreased in case of DM by ACE inhibitors which decrease the
glomerular pressure and decreased progression to renal failure.
35) All of the following are complications of chronic renal failure, except:
A. Hyperkalemia
B. Alkalosis
C. Anemia
D. Hypertension
E. Renal osteodystrophy
Answer: B* Alkalosis
Dr. Amjad Al-Afeef … 0798843824 … Amman, Jordan
Description:
In renal failure; there will be excess uric acid in the blood that cant be excreted by kidneys
leading to metabolic acidosis with wide anion gap.
Hypertension due to peripheral arterial vasoconstriction, due to the fact that kidneys are
regulating blood pressure but now losing their normal function.
Anemia of chronic disease can manifest in chronic renal failure
Renal osteodystrophy results from hyperparathyroidism due to both hypocalcemia nad
hyperphosphatemia in patient with chronic renal failure.
36) Complications of chronic renal failure include all of the following, except:
A. Peripheral neuropathy
B. Pericardial involvement
C. Hypercalcemia
D. Anemia
E. Proximal myopathy
Answer: D* Hypercalcemia
Description:
Hypocalcemia not hypercalcemia which occur in case of renal failure.
Substances that increase include:
- Potassium
- Uric acid
- Uria
- Creatinine
- Phosphorus
Substances that become low include:
- Sodium
- Calcium
37) In chronic renal failure the serum concentration of the following substances is
increased, except:
A. Uric acid
B. Calcium
C. Urea
D. Creatinine
E. Phosphorus
Answer: B* Calcium
Description:
Hypocalcemia not hypercalcemia which occur in case of renal failure.
Substances that increase include:
- Potassium
- Uric acid
- Uria
- Creatinine
- Phosphorus
Substances that become low include:
- Sodium
- Calcium
Answer: D* Digoxin
Description:
Drugs cause about 70% of AIN, they include:
(Penicillin, PPI's, Phenytoin, Cephalosporin, Sulfa drugs, Rifampicin, NSAID's, Furosemide,
Quinolones, streptomycin, Allopurinol).
Medications that are associated with AIN are the same medications that are associated with,
Drug allergy and rash, Stevens-Johnson syndrome, Toxic epidermal necrolysis and Hemolysis
Description:
Adult PKD or autosomal dominant PKD is an autosomal dominant disease resulting from
PKD1 or PKD2 gene mutations leading to formation of multiple renal cysts that manifest in
adulthood.
This condition is associated with cyst formation in another parts of the body:
- Liver cysts (most common site outside kidneys)
- Seminal vesicle cysts
- Pancreatic cysts
- Aortic root dilatation, aortic dissection
- Mitral valve prolapse, Tricuspid incontinence
- Berry aneurism (in the Circle of Willis) risk of Subarachnoid hemorrhage
It is not associated with DIC.
This condition may result in End stage renal disease.
40) In the polycystic disease of the kidney presenting in adulthood all of the following
are true, except:
A. It is inherited as an x-linked
B. It can cause hypertensive heart disease
C. It is associated with cysts of the liver and pancreas
D. It is associated with aneurysm of the circle of Wills
E. It commonly cause microscopic hematuria
Description:
ADPKD (adult type PKD) is an autosomal dominant disease not X-linked.
Cyst can compress the afferent arterioles leading to hypoperfusion of the nephrons resulting
in activation of renin angiotensin system and cause HTN
Flank pain and hematuria with HTN may ba a presentation
This condition is associated with cyst formation in another parts of the body:
- Liver cysts (most common site outside kidneys)
- Seminal vesicle cysts
- Pancreatic cysts
- Aortic root dilatation, aortic dissection
- Mitral valve prolapse, Tricuspid incontinence
- Berry aneurism (in the Circle of Willis) risk of Subarachnoid hemorrhage
Description:
Renin is a hormone secreted by Juxtaglomerular apparatus in nephron in response to
hypoperfusion on renal arteries.
It is responsible for activation of Angiotensin converting enzyme which convert angiotensin I
to angiotensin II resulting in the following:
- Secretion of aldosterone sodium and water retention
- Sympathetic activation arterial vasoconstriction
- Sodium, chloride and water reabsorption with potassium excretion
- Release of ADH from pituitary gland water reabsorption
These mechanisms will lead to increase blood pressure.
Acid-Base Balance.
42) 35 years old male presented with dyspnea (history of arthritis), ABGs showed pH
7.2, CO2 20, HCO3 12, Na 140, Cl 103, K 4.1. The acid base imbalance is:
A. Metabolic acidosis
B. Metabolic acidosis and respiratory alkalosis
C. Metabolic alkalosis and respiratory acidosis
D. Metabolic acidosis and respiratory acidosis
E. Normal ABG
Description:
Here is a tips for ABG’s reading:
Quick points:
- Increased CO2 Acid
- Increased HCO3 alkaline
- PH < 7.35 acidosis
- PH > 7.45 alkalosis
Normal values:
- Normal PH = 7.35 – 7.45
- Normal CO2 = 35 – 45 mmHg
- Normal HCO3 = 22 – 28 MEq/l
Interpretation:
- If HCO3 are changes at the same direction of PH metabolic
- If HCO3 are changes at the opposite direction of PH respiratory
Additional step to do in ABG’s reading:
Disorder Estimated change
Metabolic acidosis PaCO2 = [1.5*HCO3+8] ± 2
Metabolic alkalosis Change in PaCO2 = change in HCO3
Acute respiratory acidosis 10*change in Paco2 = change in HCO2 = 0.08 * change in PH
Chronic respiratory acidosis 10*change in Paco2 = 3* change in HCO2 = 0.03 * change in
PH
Acute respiratory alkalosis 10* change in PaCO2 = 2* change of HCO3
Chronic respiratory 10* change in PaCO2 = 5* change of HCO3
alkalosis
If the calculated Paco2 not equal to the estimated result second acid base disorder coexist
43) ABGs showed pH 7.2, PCO2 23, HCO3 16, PO2 85. The acid base imbalance is:
A. Metabolic alkalosis and respiratory acidosis
B. Metabolic acidosis and respiratory alkalosis
C. Metabolic alkalosis and respiratory alkalosis
D. Normal ABG
E. Metabolic acidosis and respiratory acidosis
Answer: B* Metabolic acidosis and respiratory alkalosis
Description:
Here is a tips for ABG’s reading:
Quick points:
- Increased CO2 Acid
- Increased HCO3 alkaline
- PH < 7.35 acidosis
- PH > 7.45 alkalosis
Normal values:
- Normal PH = 7.35 – 7.45
- Normal CO2 = 35 – 45 mmHg
- Normal HCO3 = 22 – 28 MEq/l
Interpretation:
- If HCO3 are changes at the same direction of PH metabolic
- If HCO3 are changes at the opposite direction of PH respiratory
Additional step to do in ABG’s reading:
Disorder Estimated change
Metabolic acidosis PaCO2 = [1.5*HCO3+8] ± 2
Metabolic alkalosis Change in PaCO2 = change in HCO3
Acute respiratory acidosis 10*change in Paco2 = change in HCO2 = 0.08 * change in PH
Chronic respiratory acidosis 10*change in Paco2 = 3* change in HCO2 = 0.03 * change in
PH
Acute respiratory alkalosis 10* change in PaCO2 = 2* change of HCO3
Chronic respiratory 10* change in PaCO2 = 5* change of HCO3
alkalosis
If the calculated Paco2 not equal to the estimated result second acid base disorder coexist
44) In a patient with metabolic acidosis, Serum bicarbonate 10, Sodium 130, chloride
110, Blood glucose 79, Urea 20, the anion gap in this patient is:
A. 5
B. 10
C. 15
D. 20
E. 25
Answer: B* 10
45) All of the following can cause metabolic acidosis with anion gap, except:
A. Renal failure
B. Diabetic ketoacidosis
C. Lactic acidosis
D. Aspirin overdose
E. Renal tubular acidosis
Description:
Diarrhea and RTA are the most important causes of metabolic acidosis with normal anion gap
Check the following list:
Causes of metabolic acidosis with wide anion gap (MUDPILS):
- Methanol overdose
- Uremia: renal failure
- DKA
- Phosphate, paraldehyde, propylene glycol
- Ischemia
- Lactate: hypotension, hypoperfusion
- Starvation, Salicylate overdose
Causes of metabolic acidosis with normal anion gap (DURHA):
- Diarrhea
- Urethral diversion
- Renal tubular acidosis (RTA)
- Hyperalimentation
- Addison’s disease
Answer: E* Vomiting
Description:
In vomiting, there will be a loss of HCl from stomach.
This loss in acidity will lead to metabolic alkalosis.
Other mentioned causes are known to cause metabolic acidosis. Check the following list:
Causes of metabolic acidosis with wide anion gap (MUDPILS):
- Methanol overdose
- Uremia: renal failure
- DKA
- Phosphate, paraldehyde, propylene glycol
- Ischemia
- Lactate: hypotension, hypoperfusion
- Starvation, Salicylate overdose
Causes of metabolic acidosis with normal anion gap (DURHA):
- Diarrhea
- Urethral diversion
- Renal tubular acidosis (RTA)
- Hyperalimentation
- Addison’s disease
Description:
Loop diuretics cause a net increase in bicarbonate in blood leading to metabolic alkalosis not
acidosis
Salicylates stimulate respiratory centers in the medulla, causing primary respiratory alkalosis,
which is often unrecognized in young children. Salicylates simultaneously and independently
cause primary metabolic acidosis. Eventually, as salicylates disappear from the blood, enter
the cells, and poison mitochondria, metabolic acidosis becomes the primary acid-base
abnormality.
So salicylate will cause respiratory alkalosis followed by metabolic acidosis.
Metformin and DKA will cause wide anion gap metabolic acidosis
Diarrhea is a cause of normal anion gap metabolic acidosis.
Description:
Pyloric stenosis is a cause of vomiting which will lead to loss the acid HCl from stomach
leading to metabolic alkalosis not acidosis.
Check the following list:
Causes of metabolic acidosis with wide anion gap (MUDPILS):
- Methanol overdose
- Uremia: renal failure
- DKA
- Phosphate, paraldehyde, propylene glycol
- Ischemia
- Lactate: hypotension, hypoperfusion
- Starvation, Salicylate overdose
Causes of metabolic acidosis with normal anion gap (DURHA):
- Diarrhea
- Urethral diversion
- Renal tubular acidosis (RTA)
- Hyperalimentation
- Addison’s disease
Answer: A* Acidosis
Description:
Prolonged diarrhea lead to alkaline loss and results in normal anion gap metabolic acidosis,
and hypokalemia.
Hypernatremia may result from dehydration to a patient with diarrhea
Hematocrit will not be affected unless bloody diarrhea present.
Description:
Pyloric stenosis is a cause of vomiting which will lead to loss the acid HCl from stomach
leading to metabolic alkalosis not acidosis.
DKA will accumulate the acidic ketone bodies leading to wide anion gap metabolic acidosis
Urate in renal failure and lactate in shock states are responsible for the wide anion gap
metabolic acidosis
Small intestinal fistula will lead to alkaline lose from intestine and results in metabolic
acidosis.
51) A 45 years old patient with severe nephritic syndrome is admitted with nausea, fever
and vomiting. BP is 90/50 mmHg, HR 110/m, RR 20/m, pH 7.05, PaCO2 32mmHg,
Na 132mmol/L, K 4.0mmol/L, Cl 103mmol/L, HCO3 17mmol/L, albumin 1.5g/dl,
BUN 20mg/dl, Creatinine 1.4mg/dl. One of the following acid base disorders is
present:
A. Anion gap metabolic acidosis
B. Non anion gap metabolic acidosis
C. Non anion gap metabolic acidosis and respiratory alkalosis
D. Anion and non anion gap metabolic acidosis
E. None of the above
Description:
First step in this question is to interpret ABG’s
Here PH indicates acidosis with Bicarbonate in the same direction guiding us to metabolic
acidosis.
In metabolic acidosis; PaCo2 should be equal to [1.5*bicarb + 8] ±2
Then: 32 must equal to [1.5*17+8] ±2
32 must equal to [25.5+8] ±2
32 = 33.5 ± 2 and that is true.
This confirms the presence of metabolic acidosis with no other acid base disturbance.
The next step is to calculate anion gap which equals sodium –[bicarb+chloride]
So anion gap = 132-[103+17]
Anion gap = 132 – 120
Anion gap = 12
Since the normal anion gap is 6-12
So this is a non-anion gap metabolic acidosis and the answer is B
Description:
As hyperventilation will lead to CO2 wash then it wash out an acid outside the body
leading to alkalosis caused by respiratory process. (respiratory alkalosis)
Remember this points:
Hyperventilation cause respiratory alkalosis
Alkalosis cause hypoventilation.
Hypoventilation caused respiratory acidosis
Acidosis cause hyperventilation
Hypernatremia.
53) Hypernatremia is known to occur in which of the following:
A. Syndrome of Inappropriate ADH Secretion (SIADH)
B. Diabetes insipidus
C. Renal failure
D. Hypothyroidism
E. Addison's disease
Description:
in DI; low amount or unresponsiveness to ADH makes body lose moe water leaving highly
concentrated blood with hypernatremia.
In SIADH; high amount of ADH retain water leading to dilution and low sodium
concentration
Renal failure is a cause of hyperkalemia, hyponatremia, hypocalcemia and
hyperphosphatemia.
Addison’s disease is a disease of low cortisol level leading to hyponatremia and hypotension.
Hypothyroidism cause increased ADH secretion and decreased GFR leading to hyponatremia.
Answer: A* Na – Sodium
Description:
Cation means (positive charge) while anion mean (negative charge)
The highest positive charge concentration outside cells is sodium so it is the main
extracellular cation.
The main intracellular cation is potassium
Chloride and HCO3 are anion not cations.
55) All of the following are common clinical features in cases of severe hypernatremia,
except:
A. Dry mucous membranes
B. Hypothermia
C. Delirium
D. Tachycardia
E. Hypotension
Answer: B* Hypothermia
Description:
Hypernatremia is usually related to dehydration, thirst, dry mucous membranes, hypotension
and tachycardia.
Sodium disturbances is related to brain function and may cause change in level of
consciousness.
Hypothermia is not a feature of hypernatremia.
Hyponatremia.
56) Hyponatremia can present with all the following except:
A. Restlessness
B. Headache
C. Increased appetite
D. Seizures
E. Weakness
Description:
In hyponatremia; neurological and musculoskeletal manifestations occur along with decreased
appetite not increase appetite.
Features of hyponatremia include nausea and vomiting, headache, short-term memory loss,
confusion, lethargy, fatigue, loss of appetite, irritability, muscle weakness, spasms or cramps,
seizures, and decreased consciousness or coma.
57) All of the following statements are correct about hyponatremia, except:
A. Sodium serum level of 132mEq/L is considered hyponatremia
B. It can be a manifestation of adrenogenital syndrome
C. When correcting hyponatremia, body weight is important in calculating the deficit
D. Hyponatremia does not cause convulsions
E. It may associate with inappropriate antidiuretic hormone syndrome
Description:
Features of hyponatremia include nausea and vomiting, headache, short-term memory loss,
confusion, lethargy, fatigue, loss of appetite, irritability, muscle weakness, spasms or cramps,
seizures, and decreased consciousness or coma.
Normal serum sodium is 135-145mEq/l so a level of 132mEq/l considered hyponatremia.
Adrenogenital syndrome or also known as congenital adrenal hyperplasia can cause
hyperkalemia, hyponatremia and hypotension.
To calculate sodium deficit = Sex * Weight * (desired sodium – serum sodium)
Sex = 0.6 for male and 0.5 for female.
So body weight is important to calculate sodium deficit.
In SIADH: more ADH lead to more water reabsorption and dilutional hyponatremia develop.
Answer: D* Hyperkalemia
59) Which of the following statements concerning clinical and laboratory findings in
patients with inappropriate secretion of antidiuretic hormone (SIADH) is correct:
A. High serum sodium
B. Low urine sodium
C. Low blood pressure
D. May lead to seizures
E. Evidence of dehydration
Description:
In SIADH; high level of ADH lead o increased water reabsorption leading to
- Low serum sodium may lead to seizures.
- Low serum osmolality
- High urine sodium
- High urine osmolality
- ADH lead to vasoconstriction and increased blood pressure.
- No evidence of dehydration and serum potassium will be normal
Hyperkalemia.
60) 50 years old male patient of DM, HTN, IHD, on the following medications, Statin,
insulin, beta blocker, and ACE inhibitors started recently. After 2 weeks he
presented with weakness, and the labs showed K 7.1, FBS 300, and CPK 300. The
most likely cause of hyperkalemia is:
A. Hyperglycemia
B. Rhabdomyolysis due to statins
C. ACE inhibitors
D. HTN
E. IHD
Description:
ACE inhibitors cause an inhibition of the enzyme that convert angiotensin I to angiotensin II
leading to prevent sodium water retention and lowering blood pressure.
Side effects of ACEI include hyperkalemia which is the most likely in this case
Hyperglycemia of 300mg/dl will not cause hyperkalemia, but if much higher and DKA
develop it can be a cause.
In rhabdomyolysis a CPK of 300 is unlikely and usually become elevated more than 10 times.
HTN and IHD here are distracters and no a direct cause of hyperkalemia.
61) All of the following are used in the treatment of hyperkalemia, except:
A. Calcium resonium
B. Sodium bicarbonate
C. Amiloride
D. Salbutamol
E. Calcium gluconate IV
Answer: C* Amiloride
Description:
Amiloride ia a potassium sparing diuretic that increase serum potassium, it is used to prevent
and treat hypokalemia not hyperkalemia.
Treatment of hyperkalemia include:
- Cardiac monitoring and accurate intervention if arrhythmia occur
- Restrict potassium diet
- Stabilize cell membrane:
o Calcium gluconate 10% 10ml over 10 minutes (Indicated if there is ECG
changes or if serum potassium > 7mEq/l )
- Shift potassium to intracellular space:
o Insulin 5U in 50ml of 50% dextrose solution
o Beta agonist nebulizer
o Sodium bicarbonate (if acidosis present)
- Remove Potassium by kidneys:
o Furosemide injection
o Dialysis if refractory hyperkalemia
- Remove Potassium in intestinal tract
o Kayexalate "sodium polystyrene sulfate" oral or enema – Slow onset (1-2
hrs)
o Calcium resonium "calcium polystyrene sulfate"
Answer: E* Hyperkalemia
Description:
Hyperglycemia can result in hyperosmolar coma, while hypoglycemia is known to cause
coma because sugar is the main fuel of the brain.
Potassium disorder in high or low amounts can lead to neurological manifestations including
coma.
Hypo and hyperkalemia cause muscular and cardiac symptoms but not neurological
symptoms.
Description:
ECG findings in hyperkalemia include:
- Low or absent P wave
- Prolonged PR interval
- Wide QRS complex
- Tall T wave
- Sine wave (severe hyperkalemia)
- Cardiac arrhythmias
Note that absent or flat T wave may present in case of hypokalemia.
Answer: C* Captopril
Description:
In this question of Jordan Medical council (JMC) there is two correct answers.
Captopril is an ACE inhibitor that can cause hyperkalemia.
As well as propranolol that is a beta blocker also can cause hyperkalemia.
Hyperkalemia secondary to beta-adrenergic receptor blockade occurs in 1-5% of patients and
is likely to develop with non-cardio-selective beta-blockers.
This is much confusing for you but never mind; if this question repeated again so the answer
will be captopril as it way more common to cause hyperkalemia.
Remember that these questions are not officially transmitted to us but remembered by intern
doctors who were in exam before and a mistake can happen.
Answer: C* Corticosteroids
Description:
Steroid therapy lead to sodium and water retention with loss of potassium in urin leading to
hypernatremia, hypertension and hypokalemia.
Spironolactone and amiloride are a potassium sparing diuretics which cause hyperkalemia
ACEI inhibit conversion of angiotensin I to angiotensin II leading to less sodium and water
retention, lowering in blood pressure and increased potassium reabsorption leading to
hyperkalemia.
Because potassium is the main intracellular cation so in blood transfusion, a destruction of
RBC’s will lead to large amount of potassium expelled to plasma and increase serum
potassium level leading to hyperkalemia.
66) All of the following are used in the treatment of hyperkalemia, except:
A. I.V glucose plus soluble insulin
B. I.V 10% calcium gluconate
C. I.V sodium bicarbonate
D. Dialysis
E. Amiloride
Answer: E* Amiloride
Description:
Amiloride ia a potassium sparing diuretic that increase serum potassium, it is used to prevent
and treat hypokalemia not hyperkalemia.
Treatment of hyperkalemia include:
- Cardiac monitoring and accurate intervention if arrhythmia occur
- Restrict potassium diet
- Stabilize cell membrane:
o Calcium gluconate 10% 10ml over 10 minutes (Indicated if there is ECG
changes or if serum potassium > 7mEq/l )
- Shift potassium to intracellular space:
o Insulin 5U in 50ml of 50% dextrose solution
o Beta agonist nebulizer
o Sodium bicarbonate (if acidosis present)
- Remove Potassium by kidneys:
o Furosemide injection
o Dialysis if refractory hyperkalemia
- Remove Potassium in intestinal tract
o Kayexalate "sodium polystyrene sulfate" oral or enema – Slow onset (1-2
hrs)
o Calcium resonium "calcium polystyrene sulfate"
Description:
Treatment of hyperkalemia include:
- Cardiac monitoring and accurate intervention if arrhythmia occur
- Restrict potassium diet
- Stabilize cell membrane:
o Calcium gluconate 10% 10ml over 10 minutes (Indicated if there is ECG
changes or if serum potassium > 7mEq/l )
- Shift potassium to intracellular space:
o Insulin 5U in 50ml of 50% dextrose solution
o Beta agonist nebulizer
o Sodium bicarbonate (if acidosis present)
- Remove Potassium by kidneys:
o Furosemide injection
o Dialysis if refractory hyperkalemia
- Remove Potassium in intestinal tract
o Kayexalate "sodium polystyrene sulfate" oral or enema – Slow onset (1-2
hrs)
o Calcium resonium "calcium polystyrene sulfate"
Description:
Ringer’s lactate contains 4mEq/l potassium and it is not suitable for treating hyperkalemia
Treatment of hyperkalemia include:
- Cardiac monitoring and accurate intervention if arrhythmia occur
- Restrict potassium diet
- Stabilize cell membrane:
o Calcium gluconate 10% 10ml over 10 minutes (Indicated if there is ECG
changes or if serum potassium > 7mEq/l )
- Shift potassium to intracellular space:
o Insulin 5U in 50ml of 50% dextrose solution
o Beta agonist nebulizer
o Sodium bicarbonate (if acidosis present)
- Remove Potassium by kidneys:
o Furosemide injection
o Dialysis if refractory hyperkalemia
- Remove Potassium in intestinal tract
o Kayexalate "sodium polystyrene sulfate" oral or enema – Slow onset (1-2
hrs)
o Calcium resonium "calcium polystyrene sulfate"
Hypokalemia.
69) 55 years old male presented with generalized muscle weakness, he recently started
Lasix. The most likely electrolyte disturbance is:
A. Hyperkalemia
B. Hypokalemia
C. Hypernatremia
D. Hyponatremia
E. Hypocalcemia
Answer: B* Hypokalemia
Description:
Lasix (furosemide) is a loop diuretic that is widely used.
Its side effects include electrolyte disturbances including hyperkalemia and hyponatremia.
We now know that hyponatremia will cause neurological symptoms while hypokalemia will
cause muscle and cardiac symptoms.
Our patient has muscle weakness so the most likely diagnosis is hypokalemia.
Description:
Decreased intestinal mobility can occur but not colic
Muscular weakness and decreased deep tendon reflexes are the main features of hypokalemia
Here is the main manifestations of hypokalemia:
- Fatigue, weakness , cramps, paralysis, anorexia, nausea, vomiting
- Decreased bowl mobility (ileus)
- Hyperglycemia: due to suppressed insulin
- Restless legs
- Rhabdomyolysis
- Arrhythmias
- Hypotension (due to decreased peripheral resistance)
- ECG changes: (ST depression, broad and flat T wave, U wave)
- Metabolic alkalosis
71) All the following are manifestations of hypokalemia, except:
A. Drowsiness
B. Muscular hyperreflexia
C. Listlessness and slurring of speech
D. Depressed S-T segment in ECG
E. Sluggish or absent intestinal movements
Description:
Muscular weakness and decreased deep tendon reflexes are the main features of hypokalemia
Here is the main manifestations of hypokalemia:
- Fatigue, weakness , cramps, paralysis, anorexia, nausea, vomiting
- Decreased bowl mobility (ileus)
- Hyperglycemia: due to suppressed insulin
- Restless legs
- Rhabdomyolysis
- Arrhythmias
- Hypotension (due to decreased peripheral resistance)
- ECG changes: (ST depression, broad and flat T wave, U wave)
- Metabolic alkalosis
Description:
In tumor lysis syndrome there will be cellular destruction with hyperkalemia, hyperuricemia
and hyperphosphatemia along with hypocalcemia.
Renal tubular acidosis types I and II are associated with hypokalemia while type IV
associated with hyperkalemia.
Muscular paralysis and paralytic ileus are manifestations of hypokalemia.
Bartter’s syndrome is an inherited disease (in autosomal recessive pattern) leading to
hypokalemia due to impairment of Sodium, potassium, 2 chloride co-transporter (NKCC2) in
the ascending loop of Henle.
Description:
In acute renal failure; hyperkalemia, hyperphosphatemia, hypocalcemia and hyponatremia
develop.
The other mentioned choices are a causes of potassium loss in intestine, and cause
hypokalemia.
74) All of the following can cause hypokalemia, except:
A. Vomiting
B. Chronic laxative ingestion
C. Cushing's syndrome
D. Renal failure
E. Diuretic therapy
Description:
In renal failure; hyperkalemia, hyperphosphatemia, hypocalcemia and hyponatremia develop.
Vomiting, laxative ingestion is a cause of potassium loss from GI tract leading to
hypokalemia
In Cushing's syndrome there will be hypokalemia along with hyperglycemia, metabolic
alkalosis and hypertension.
Diuretic therapy can cause hypokalemia except a potassium sparing diuretics like Amiloride
and spironolactone (Aldactone) which cause hyperkalemia.
Description:
Captopril is an ACE inhibitor which cause hyperkalemia not hypokalemia.
Vomiting and diarrhea lead to potassium loss from GI tract resulting in hypokalemia.
In Cushing's and Conn’s syndrome there will be hypokalemia along with metabolic alkalosis
and hypertension.
High insulin intake will lead to potassium shifting to intracellular space leading to low plasma
potassium (hypokalemia)
Answer: C* Spironolactone
Description:
Spironolactone (Aldactone) as well as Amiloride are a potassium sparing diuretics which
cause hyperkalemia
Other mentioned choices are a cause of hypokalemia.
Hypercalcemia.
77) All of the following are causes of hypercalcemia, except:
A. Acute pancreatitis
B. Sarcoidosis
C. Multiple myeloma
D. Cancer of lungs
E. Hyperparathyroidism
Description:
In acute pancreatitis, calcium will bind to free fatty acids that result from reaction between
pancreatic enzymes and abdominal tissues leading to hypocalcemia.
In sarcoidosis: macrophages will activate vitamin D3 in granuloma leading to increase
calcium absorption (from intestine) and reabsorption (from kidneys) leading to hypercalcemia
Parathormone excess in case of hyperparathyroidism or ectopic secretion from lung cancer
will lead to calcium absorption (from intestine), reabsorption (from kidneys), and resorption
(from bone) leading to high serum calcium (hypercalcemia).
In multiple myeloma: increased osteoclastic activation, elevated Parathormone related protein
(PTH-rp) and increase calcium reabsorption in renal tubules leads to hypercalcemia.
Description:
In acute pancreatitis, calcium will bind to free fatty acids that result from reaction between
pancreatic enzymes and abdominal tissues leading to hypocalcemia.
In sarcoidosis: macrophages will activate vitamin D3 in granuloma leading to increase
calcium absorption (from intestine) and reabsorption (from kidneys) leading to hypercalcemia
Parathormone excess in case of hyperparathyroidism or ectopic secretion from lung cancer
will lead to calcium absorption (from intestine), reabsorption (from kidneys), and resorption
(from bone) leading to high serum calcium (hypercalcemia).
Hypervitaminosis D will increase calcium absorption (from intestine) and reabsorption (from
kidneys) leading to hypercalcemia
Description:
In Medullary thyroid cancer; increased level of calcitonin will lead to hypocalcemia.
Calcitonin is a hormone secreted from C-cells in thyroid gland which oppose the action of
parathormone. Remember that Medullary thyroid cancer is a part of MEN type I and II.
Squamous cell carcinoma of the lung is known to secret ectopic PTH leading to
hypercalcemia.
In thyrotoxicosis hypercalcemia results from direct effect of thyroxine on the bone.
Milk alkali syndrome characterized by high serum calcium and metabolic alkalosis due to
ingestion of calcium and absorbable alkali (example: food and antacids)
In Addison’s disease; Volume depletion lead to increase reabsorption of calcium in kidneys
leading to hypercalcemia.
Description:
In acute pancreatitis, calcium will bind to free fatty acids that result from reaction between
pancreatic enzymes and abdominal tissues leading to hypocalcemia.
Parathormone excess in case of hyperparathyroidism will lead to calcium absorption (from
intestine), reabsorption (from kidneys), and resorption (from bone) leading to high serum
calcium (hypercalcemia).
In sarcoidosis: macrophages will activate vitamin D3 in granuloma leading to increase
calcium absorption (from intestine) and reabsorption (from kidneys) leading to hypercalcemia
Milk alkali syndrome characterized by high serum calcium and metabolic alkalosis due to
ingestion of calcium and absorbable alkali (example: food and antacids)
81) All of the following are useful in the acute treatment of hypercalcemia, except:
A. Hydration using intravenous saline solution
B. Furosemide
C. Hydrochlorothiazide
D. Mithramycin
E. Calcitonin
Answer: C* Hydrochlorothiazide
Description:
Thiazide diuretics are a cause of hypercalcemia and cant be a treatment for it.
Treatment of hypercalcemia include:
- I.V normal saline (first line)
- Furosemide (Lasix) – use with caution.
- Calcitonin has faster effect than Bisphosphonates
- Bisphosphonates (inhibit bone resorption)
- Surgical removal of adenoma
- Mithramycin (used to treatment of hypercalcemia in malignancy)
- Steroids (treat hypercalcemia in sarcoidosis)
Hypocalcemia.
82) All of the following are side effects of furosemide, except:
A. Hypokalemia
B. Hyperuricemia
C. Hyperglycemia
D. Ototoxicity
E. Hypercalcemia
Answer: E* Hypercalcemia
Description:
Hypocalcemia, hypocalcemia, hypomagnesemia, hyponatremia, hypochloremia and metabolic
alkalosis are side effects of furosemide
Uric acid and glucose may increase.
It is also ototoxic (cause irreversible deafness) and nephrotoxic (cause acute interstitial
nephritis)
Description:
celiac disease will lead to malabsorption of vitamin D leading to hypocalcemia.
In osteoporosis, osteopetrosis and paget disease of bone; serum calcium will be normal
Vitamin D intoxication and primary hyperparathyroidism is a cause of hypercalcemia
Don’t be confused with secondary hyperparathyroidism which is increased PTH in response
to hypocalcemia.
Hypercalcemia is acromegaly is related to presence of associated hyperparathyroidism (as a
case of MEN type I)
Answer: D* Pseudopseudohypoparathyroidism
Description:
Slow tendon reflexes is a feature of hypokalemia not hypocalcemia.
Signs and symptoms of hypocalcemia include:
- In children: (carpopedal spasm, stridor, convulsions)
- An adults: tingling in hand feet and around mouth, Muscle cramps, Psychosis,
abdominal cramps
- Trousseaus sign (carpal spasm after inflation of cuff on arm)
- Chvostek's sign (twitching of facial muscles after facial nerve tapping)
- Peroneal sign (taping on Peroneal nerve results in dorsiflexion and abduction of foot)
- Erb's sign (motor nerve can be stimulated by low current <5 milliampere)
- Prolonged QT interval in ECG
Phosphate
86) The serum alkaline phosphatase level is characteristically normal in:
A. Hemolytic jaundice
B. Osteomalacia
C. Osteitis deformans
D. Hypophosphatasia
E. Primary hyperparathyroidism
Description:
In hemolytic jaundice, alkaline phosphatase will be normal. It will be elevated in obstructive
jaundice.
High alkaline phosphatase may present in bone diseases like osteomalacia, osteitis and
Paget’s disease
Alkaline phosphatase will be high in chronic kidney disease, primary hyperparathyroidism as
well as hypophosphatemia.
Alkaline phosphatase will be normal in osteoporosis and osteopetrosis as well as in
intrahepatic and prehepatic jaundice.