Midterm Flashcards
“A 56 year old woman complaints of fatigue. Accodring to her medical records, she has HT, peptic ulcer and nephrolithiasis.
Laboratory findings:
se[Ca]: 2,8 mmol/L
se [PO4]: 0,6 mmol/L
se[ALP]: 450 U/L
DEXA scan: T-score of -2,8 SD on the hip and forarm
What tests would you order to determine the exact cause of her disease?”
Hypercalcemia: nephrolithiasis and fatigue
Hypophosphatemia:
ALP of 450: should be < 150 –> indicates osteoclast activity.
Osteoporotic T score (normal >-1.0, Measured by DEXA
Diagnosis: Primary hyperparathyroidism (oversecretion of PTH, can be caused by adenoma or hyperplasia)
Osteoporosis bc of PTH –> osteoblast activity increase –> bone resorption increase
PTH increase osteoclast activity -> Ca2+ increase
PTH increases production of Vit.D, and thus phosphate decrease
Additional tests:
- Scintigraphy with 99Tc
- US
- PTH and Vit.D levels
- Biopsy
“A 68 year old non-smoking man has been complaining of progressive weakness for 2 weeks. In addition to these symptoms he has developed intermittent cough, pleuritic chest pain and excretional dyspnea for 6 days. In the last weeks he frequently experienced nausea and vomited several times. Medical history reveals no HT or coronary heart disease. He has a long history of heartburn - he takes regularly antacids and drinks 1-2 L milk/ day.
Laboratory findings: se Ca: 2.8 mmol/L se Phosphate: 1.8 mmol/L BUN: 24 mmol/L HCO3: 38 mmol/L PTH and Vit.D: normal
What is the most likely diagnosis?”
MILK ALKALI SYNDROME: chronic ingestion of high amount og antacids + hypercalcemia are strong clues
Hypercalcemia:
- ingested too much bicarb.
- CNS depressing effect
Hyperphosphatemia: . PTH is normal and so phosphat excretion is normal. More sticks around to bind Ca
High BUN: 2-10 er vanlig.
- kidney failure due to milk-alkali syndrome bc. og nephrocalcinosis
High bicarb: over-absorption –> mild alkalosis
Since PTH and Vit. D are normal = other causes ruled out - ie. hyperparathyroidism
“A 35 year old woman is complaining about frequent muscle cramps. She was admitted to the hospital after having a convulsion. She had thyroidectomy 3 months ago and she is on thyroid hormone substitutions since then. Physical examination revealed a positive Chvosteks signa and Trousseaus phenomenon.
Laboratory findings:
se [Ca]: 1 mmol/L
se[PO4]: 2.0 mmol/L
serum ALP: 140 U/L
What is your diagnosis? What further tests would you order to support your diagnosis?”
Diagnosis: PTH deficiency due to thyroidectomy where the parathyroids glands also were removed whilst removing the parathyroids.
Severe hypocalcemia:
- hyperflexible muscles, muscle cramping and convulsions (chevostek and Trossaus signs)
Chevostek: twitching masseter muscle
Trossaus phenomenom: inflate BP-cuff–> forarm contract/spasms
Hyperphosphataemia:
- PTH stimulates phosphate excretion. Without PTH –> Phosphate increase
Further tests:
- PTH levels
- Imaging
“A 66 year old woman felt a sharp, sudden lumbar pain as she was lifting a bag of groceries out of the supermarket cart. An X-ray taken in the emergency showed a compression fracture of L1.
Laboratory findings:
se[Ca]: 2,4 mmol/L
se[PO4]: 1,1 mmol/L
What is your diagnosis? What further tests should you order?”
Pathological fracture –> likely due to primary (postmenopausal) osteoporosis
Estrogen stimulates OPG production, and OPG decreases osteoclast activity. Low estrogen –> overactive osteoclasts –> extensive bone remodeling
If it was osteomalacia: Ca and Pi would be low
If she had hyperparathroidism: Ca high, Phos low (or high) depending on origin
Tests:
DEXA: see T-score to diagnose osteoporesis
Labs:
- PTH, ALP, urinary calciym and phosphate (all should be normal)
- Check estrogen
“A 60 year old diabetic woman has been on hemodialysis for 15 years. She recently started to complain about cardiac pain. She has no history of cardiac illness. Physical examination reveals pale, grey-yellow colored skin, but nothing else remearkable. Exercise electrocardiogram shows ST-T alterations.
Laboratory findings: ALAT: 45 U/L ASAT: 52 U/L serum creatinine: 180 umol/L serum Ca: 2,1 mmol/L serum phosphate: 2,8 mmol/L serum PTH: elevated
What is the possible diagnosis? What further tests would you perform?”
RF with secondary hyperparathyroidism: damage kidney cannot remove enough phosphate –> hyperphosphatemia –> bind free Ca –> free Ca decrease —> stimulate PTH secretion.
Hypocalemia also occur becase low vitamin D levels will reduce Ca2+ reabs
FGF-23
ALAT is normal (<45U/L)
ASAT at 52 is slightly elevated (normal < 45 U/L)
ALP is normal (150U/L)
High seCreatinine: indicate low GFR, poor kidney function
Cardiac pain: ST-T changes
Paleness:related to anemia due to decreased EPO.
Rule out AMI
US
Serum electrolytes
“A 65 year old man complains of frequent urination and urinary retention. There is no macroscopic hematuria, urination is not painful. He complains of recurrent abdominal pain in the last weeks.
Laboratory findings:
serum Ca: 3,5 mmol/L
serum PO4: 2 mmol/L
BUN: normal
What is the possible diagnosis? What further tests would you perform to support your diagnosis?”
PROSTATE CARCINOMA WITH BONE METASTASES
Prostate enlarged (no pain, no blood, no bleeding).
Severe hypercalcemia: alarmingly high -> at risk for cardiac arrest
Elevated phosphate: neoplastic bone lesion
Further test:
- Prostate evaluation
- Imaging of metastases
- ALP
- PTH
“Some weeks after having a sore throat and high fever, the patient has developed edema. His blood pressure is increased.
Urinalysis
volume: 450mL/day
protein: +++ (3g/day)
sediment: 50-100 erythrycytes/HPF, leukocytes rarely
creatinine clearance: 30 mL/min
What is the presumable diagnosis?”
RPGN - nephritic syndrome. Can be post-streptococcal. Subendothelial IC-deposition. High protein excretion can cause edema. HT due to increased renin secretion (low GFR)
Borderline oliguria. 3g protein is above normal -> due to GN.
ESR = 50-100, indicate hematuria
Creatinine clearance indicate GFR = 120-125mL/min (normally)
"Laboratory findings of a patient with massive edemas: serum total protein: 40g/L serum cholesterol: 8mmol/L ESR: 28mm/h BP: 120/80 mmHg Urinalysis: quantity: 1800mL/day protein: ++++ (12g/day) sediment: 1-2 leukocytes/hpf, erythrocytes rarely, a lot a hyaline casts What is the presumable diagnosis? "
Diagnosis: nephrotic syndrome. Higher risk of atherosclerosis
Massive edema, normal BP
Total protein is too low, due to severe kidney excretion
High cholesterol: liver tries to compensate to low serum proteins, including lipoproteins
Increased ESR
Slightly increased urine volume
SEVERE proteinemia, albumin is being lost too
Hyalin casts: not just of normal composition
"A febrile patient complaints of lumbar pain. Urinalysis: protein: ++ pus: +++ sediment: a lot of leukocytes, some erythrocytes, epithelial cells, a lot of bcteria, leukocyte casts. Ck: 100mL/min ESR: 38mm/h What is the presumble diagnosis?"
Pyelonephritis
- Moderate protein in urine, some glomerular damage
- Pyuria: WBC in urine –> UTI
- Leukocyte = infection
- RBC = damage
- Low Ccr.: impaired kidney function
- Increased ESR: in inflammation especially
Pyelonephritis is usually due to ascending UTI.
“Laboratory findings of a patient include the following:
Urinalysis:
sediment: 3-5 erythrocytes/Hpf, rarely lekocytes
the erythrocytes are isomorphic;
there is a miminal proteinuri, the urinary protein electrophoresis does not show selectivity in the proteinuria;
Ck: 120mL/min
What can be the probable diagnosis: glomerular hematuria or urinary tract bleeding?”
Mild urinary tract bleeding (3-5 RBC/hpf)
Normal morphology of RBC (if glomerular damage the RBC would be dehydrated)
Minimal proteinuria:
GFR not impaired
Diagnosis:
- mild bleeding, most likely due to smalll nephrolithiasis
"After receving a massive dose of aminoglycoside antibiotics, a patient with no prior symptoms of kidney disease develops a body weight gain of 3kg over a period of 3 days. He does not void urine spontaneously. The total volume of urine collected by catheterization is 200mL/day. Other laboratory results: serum creatinine: 440umol/L serum urea: 28,5 mmol/L plasma K+: 6.2 mmol/L What is the most likely diagnosis?"
Diagnosis: ACUTE RENAL FAILURE due to aminoglycoside toxicity
Causes ATN by the toxicity
Gained 3kg in fluids.
anuria (borderline), sudden retention problem
High creatinine = indicate RF
Hyperkalemia indicates RF
Retention parameters: hyperkalemia, high creatinine and increased serum urea.
“The serum glucose level is 15 mmol/L in a diabetic ketoacidosis. GFR is markedly decreased (20mL/min). Tubular function tests are negative. No glucose can be detected in the urine (by repeated tests).
How is this possible?”
Kimmelstein-Wilsons disease:
Negative tubular function test BUT severely decreased GFR (6th of normal) –> tubules have more time to reabsorb glucose –> no glucosuria.
Diabetic nephropathy –> diabetic angiopathy –> nodular sclerosis –> KWD.
"Laboratory findings of a patient: Urinalysis: color: straw-yellow pus: +++ transparency: turbic (nubecular) blood: + quantity: 400mL (present), 1600mL/day glucose: negative acetone: negative specific gravity: 1022 ubg: normal protein: 50mg/day bilirubin: negative Urinary sediment: 20-30 epithelial cells, 30-40 WBC, 3-4 RBC, per hpf Further data: body temperture: 38*C WBC: 12 G/L, RBC: 4,5 T/L, ESR: 2mm/h creatinine clearance: 120mL/min cultivation of E.coli: positive
What is the most likely diagnosis?”
UTI by E.coli infection
Pyuria by WBCs = infection
ESR 2 = not chronic infection
“A person fainted while working in the summer heat for a long time.
Complaints: thirst, dry mouth, weakness, oliguria
Physical examination: decreased skin turgor, blood pressure: 110/70 mmHg
Laboratory parameters:
se[Na]: 152 mmol/L
se[K]: 5 mmol/L
htc: 0,45
HGB: 160 g/L
MCV: 70 fL
How do you explain the laboratory parameters? What is to be done with the patient? “
HYPERNATREMIC HYPOVOLEMIA due to heat exhaustion. Severe dehydration.
BP sligtly low
Hypernatremia - sweat is hypOSMOTIC because of the Na-reabs. in the sweat ducts.
K+: borderline high. More fluid than electrolyte loss.
Htc is normal:
Normal hemoglobin: rules out that blood loss is the cause of the hypovolemia
Microcystosis (MCV): low. H20 pulled out by osmolar forces, leading to cell dehydration
Treatment:
- cooling
- should be given an electrolyte solution
“An elderly person gets sick while enjoying himself on Octoberfest: he complains of a headache and muscle cramps. He is disoriented. He has drunk 4 liters of beer during the past 2 hours.
Physical examination: alcoholic breath, increased plantar extensor reflex. BP: 180/100 mmHg
Laboratory parameters: se[Na]: 126mmol/L se[K]: 4 mmol/L MCV: 102 fl Htc: 0,36 se[creatinine]: 150mmol/L se [urea]: 18 mmol/L urine densityr: 1,015 kg/L; [Na]: 20 mmol/L
How do you explain the symptoms and the laboratory results?”
Urine should be more diluted, and there is a clear urine retention. All parameters suggest there is something wrong with the kidney —> most likely the whole nephron is involved. Renin disease –> affect the renin production. Babinsci reflex –>increased pressure in the skull —> risk for brain edema, will explain the neurological symptoms. The muscle cramps are due to the CNS involvement.
Lab parameters (hyponatremia) indicates a hypovolemic hyponatremia –> water poisioning–> hypoosmolarity –> also increased risk for brain edema (same reason, pressure will increase in the skull).
Beer is hypotonic w/some alcohol. Decreased htc = decreased RBC count–> water intoxication. Both creatinine and urea are high bc. if you loose concentration ability you loose dilution capability. Urine density would be “more normal” if the kidney funtion was optimal.
In a healthy person: would see normal kidney parameters, but hyponatremia (no RF-markers). Presence of RF-markers = indicate renal failure or insufficiency
“An elderly woman has been on NSAIDS treatment for a long time, because of her rheumatoid arthritis. She got very weak after having an acute diarrhea, she feels too dizzy and needs to sit down.
Physical examination: decreased skin trugor. BP in supine position = 120/80, but standing = 90/55 mmHg
Laboratory parameters: se[Na]: 116 mmol/L se [K]: 6,2 mmol/L Htc: 0,48 se[creatinine]: 180mol/L se [urea]: 18 mmol/L urine [Na]: 50 mmol/L
How do you explain the symptoms and the laboratory results?
“
Hypovolemic hyponatremia due to RF and diarrhea
- Long term use of NSAIDs can cause Renal medullary hypoxia, especially in ppl with already poor health, and have RAAS activation
When RAAS is activated –> constrict afferent arteriole, and the kidney can become hypoxic. PGE2 released in response –> dilate afferent arteriole –> restore blood flow.
NSAIDs inhibit PGE2, kidney remain hypoxic –> excrete sodium
Called ANALGESIC NEPHROPATHY
RF: explains increased sodium excretion and potassium retention.
Orthostatic HT: due to hypovolemia
Hyponatremia: due to excretion
Urinary sodium: RF sign
Hyperkalemia RF due to decreased urinary excretion of K+
Htc is high: due to hypovolemia
Azotemia
Decreased skin trugor: dehydration sign
“How will the following laboratory values be changed in a protracted, untreated diabetic ketoacidosis coma before treatment?
Total potassium of the body
Total sodium of the body
Total water (fluid) of the body
Does the serum [K] change in parallel with the potassium amount of the body? How do you think the appropriate treatment will change the serum [K] concentrations?”
DKA: a state where the body has no insulin-mediated glucose regualtion, and thus it will continue to produce glucose, although the serum levels are very high. Glucose is osmotically active, and attracts both solutes and solvents. When glucose serum limit is reached, glucose excretion by the kidneys takes both solutes and water with it
Total potassium of the body: DECREASE. Serum concentration will occur normal or high, because glucose forces i.c. potassium into the blood
Total sodium of the body: DECREASE: lost via urine
Total water of the body: DECREASE. DKA causes polyuria –> water loss
Treatment: infusion and insulin administration –> help drive K+ back into the cells.
Calcium-gluconate
Normalization of glucose will help normalization of the osmotic diuresis
“An elderly man gets chemotherapy for his chronic lymphoid leukemia. He complaints of intermittent palpitations, and being disoriented. BP: 90/60 mmHg
Laboratory paramters:
se[Na]: 135 mmol/L
se [K]: 8,2 mmol/L
Htc: 0,28
How can you explain the laboratory results? What kind of ECG abnormalities can you expect to see? What would you do with him?”
Low BP
Normonartemia
Hyperkalcemia
Critically low htc
TUMOR-LYSIS syndrome, causes K+ increase
Low htc due to BM overpopulation due to malignancy.
ECG abnormalities
- high T wave, tent like
- Prolonged PQ
- P-wave flattening, or disappears
- Wider QRS
- V-fib susceptible
Treatment:
- treat hyperkalemia
- Treat hypotension and low hematocrit
“A woman gets hospitalized after having broken several of her bones in a car accident. BP: 80/50 mmHg, HR: 130 bpm. The patient develops oliguria after being stabilized.
Laboratory parameters: se [Na]: 150 mmol/L se[K]: 7,2 mmol/L se [creatinine]: 350 umol/L se[urea]: 18,8 mmol/L htc: 0,33
Urine amount (by catheterization): 200mL. What emergency treatment is necessary? How can you explain the parameters seen later?"
CIRCULATORY SHOCK! High risk for MOF, with significant renal failure. Suspect CRUSH syndrome.
Emergency treatment:
- stop bleeding
- give calcium gluconate
- Restore BP with IV dextran
- Give bicarbonate to prevent acidosis
- Insulin + glucose: to move K+ back into cells
Blood is redistributed. Can get acute tubular necrosis
“What is the direction of change in the parameters below during respiratory acidosis?
aHCO3
stHCO3
BE
During generation and compensation”
aHCO3 will initially increase, and after compensation further increase. Dependent both metabolically and respiratory. Kidney compensate by reabs. more HCO3
stHCO3 will initially be unchanged, and after compensation increase. Only dependent on metabolism.
BE will be unchanged initially, and finally positive.
Generally: shows the base deficit reflecting the metabolic side, no change initially
Compensation: pos = base excess = lack of acids.
OBS: 6-8h needed for compensation, and up to 3-5 days for maximal effect. Need to synthesize channel proteins
“Diabetic ketoacidosis. How and why do the indicated parameters deviate from normal?
pH, pCO2, BE, aHCO3, stHCO3, AG se[K]”
pH decrease because of ketones (acidic), but will become less acidic with compensation
pCO2: related to compensation, so initially equal, but when compensation starts the pCO2 will decrease
BE: strongly negative due to lack of base, but when kidneys start to compensate the value will be a bit less negative
aHCO3: both respiratory and metabolic parameter. Increase in H+ will deplete HCO3 as a buffer, so initially it will decrease. Lung compensation, further decrease, and then a little less decrease with kidney compensation.
stHCO3: depleted as buffer, but increases with kidney compensation
AG: ketones = aniones —> high AG
seK+: INCREASED
- insulin is a stimulator of Na+/K+ ATPase –> lack of insulin will cause decreased cellular uptake.
“Traumatic shock (bleeding, crush). The acid-base parameters during the first hours and one day later:
pH: 7.2 --> 7.05 pCO2: 20 --> 55 mmHg HCO3: 8 ---> 13 mmol/L st HCO3: 11 mmol/L both times BB: 28 mEq/L both times BE: -18mEq/L both times
One day after the trauma symptoms of shock-lung develop. Identify the type and analuyze the different stages of the acid-base imbalance”
At day of accident:
PRIMARY METABOLIC ACIDOSIS with normal respiratory compensation
One day later:
METABOLIC + RESPIRATORY ACIDOSIS because the lungs cannot compensate because of ARDS
"A 35-year-old woman reports to the ED with shortness of breath. She has cyanosis of the lips. She has had a productive cough for 2 weeks. Her temperature is 39 oC, blood pressure 110/76 mmHg, heart rate 108 bpm, respirations 32/min, rapid and shallow. Breath sounds are diminished in both bases, with coarse bronchi in the upper lobes.
Her ABG results are:
pH = 7.44,
pCO2 = 28 mmHg,
aHCO3− = 18 mmol/l,
stHCO3− = 20 mmol/l,
AG = 12 mmol/l,
pO2 = 54 mmHg
How do you interpret her ABG result? What other test would you order to verify your diagnosis?"Start of resp. alkalosis due to hyperventilation in relation to pulmonary edema caused by sepsis (or pneumonia), secondary metabolic acidosis.
"A 23 year-old woman with exacerbated rheumatoid arthritis enters to the ED. She has frequently vomited lately.
Her medication: Aspirin 3–5 pills/day.
Her ABG result:
pH = 7.70,
pCO2 = 25 mmHg,
aHCO3− = 30 mmol/l,
AG = 22 mmol/l
(Calculated pCO2 = 42–44 mmHg.)
What kind of acid-base disorders does she have?"Aspirin side-effect = vomiting = GI problem = loose H+ –> increase pH.
3-5 pills = overdose!
Alkalemia, low pCO2 = alkalemia. Rapid and deep breathing.
AG is 22 –> PRIMARY METABOLIC ACIDOSIS REGARDLESS OF pH and HCO3
Additional respiratory alkalosis.
SALICYLATE POISIONING.
Primary metabolic acidosis with co-existing respiratory and metabolic alkalosis
