1 semester II random Flashcards

Question

7. Laboratory findings of a patient: _Urinalysis:_ color: straw-yellow transparency: turbid (nubecula) quantity: 400 ml (present), 1600 ml/day specific gravity: 1022 protein: 50mg/day **pus: +++** **blood: +** glucose: neg acetone: neg ubg: norm bilirubin: neg _Urinary sediment:_ 20–30 epithelial cells 30–40 WBC 3–4 RBC, per high power field _Further data:_ body temperature: 38°C WBC: 12 G/l RBC: 4.5 T/l ESR:2 mm/h creatinine clearance: 120 ml/min, cultivation of **E. coli: positive** What is the most likely diagnosis?

Answer 1

Many normal findings are listed: normal urine volume (being just above the “normal” 1.5L/day is not significant), normal specific gravity (1010-1035), no proteinuria (\< 300 mg/day), no glucosuria (no diabetes), normal UBG and bilirubin (liver is OK), body temperature on the upper end of normal but it’s not a true fever, normal RBC count (4.4-5.5 T/l), ESR is \< 20 mm/h, normal creatinine clearance (120-125 ml/min) _Diagnosis:_ **Urinary Tract Infection from E. coli that has not ascended to become pyelonephritis** Color: seems to **indicate** significant **pus** Pus +++: clear sign of **infection** **Microscopic hematuria:** very small amount of blood. Never find out if RBCs are isomorphic for sure but they probably are since there is no renal glomerular/tubular involvement. Epithelial cells in urine: also **due to damage** Elevated WBC count: (normal 4-10 G/l) - usually **increases with infection** Neutrophils in particular increase with bacterial infections **Positive E. coli** Culture: makes the diagnosis of **UTI** easy. **No signs of systemic/organ** infection → ESR is not elevated, no fever, etc. Urinary tract infections **do not normally cause fever** unless the infection reaches the kidney.

Answer 2

* This is **lactose intolerance** which can be worsened by **alcohol, because it decreases lactase activity.** * Tests : * _Lactose Hydrogen Breath Test_ - patient swallows a lactose solution and their breath ischecked every 20-30 mins for 2-3 hours against a baseline measurement for largeincreases in hydrogen gas * _Blood Glucose Test_ - lactose malabsorbers will generally see less of an increase inblood glucose after ingesting lactose * _Stool Acidity Test_ - for infants b/c they don’t cooperate with (\*\*Lactose intolerance(HBT)Alcohol - inhibits enzyme activity (worsen the symptoms)\*\*)

Answer 3

_Clinical findings:_ Type 1DM with no food intake or insulin for two days highly suggests **_diabetic ketoacidosis._** The extra stress associated with a flu can also trigger a DKA. Without insulin cells are not able to take up glucose and thus they are in starvation. The **liver** starts **producing ketone bodies** which are **acidic.** _Laboratory findings:_ [Na+] is **low** (n;135-145mM), [K+] is **high** (n:3,5-5,0 mM), [Cl-] is **low** (n:95-105 mM) As both **ketones** and **glucose** are **osmotically active,** an **increase in ECF** can explain the **low sodium** and **chloride** (relative decrease). ((( **Polyuria** would also occur due to **osmotic diuresis,** then the **kidney** would **not** be **able to reabsorb sufficient Na**+, and as Cl- is reabsorbed by electrical gradient caused by sodium it makes sense that it is also not reabsorbed sufficiently???))) **Lack of insulin decreases** the activity of **Na+/K+-ATPase** which can explain the **increase** in **potassium** _(also decrease in sodium?_). In addition, **due to high H+** concentrations in acidosis, **cells** can **use** the **H+/K+-exchanger** to take up H+ and thus **increasing EC potassium.** Fasting glucose (not eaten for two days) is too high (n:3,0-6,0), indicating that there is no uptake of glucose in the periphery and gluconeogenesis in the liver. **pH** indicates **acidemia.** * *aHCO3** - indicates a **metabolic source** for the **acidosis.** **pCO2** is **low,** indicating **respiratory compensation** **AG** (130 - (80+10)) = **40 mM**, **AG \> 20 mM** indicates **_primary metabolic acidosis_** no matter HCO3- & pCO2 values. **Expected pCO2** = **21-25** mmHg, measured pCO2 is within this range - indicating _normal respiratory compensation_ **Corrected HCO3-** = **38** mM * Because this is **\> 26 mmol/L,** it indicates **_coexisting metabolic alkalosis_** (here being the excessive vomiting, expelling stomach acid) _Conclusion:_ **Diabetic ketoacidosis** (_primary anion gap metabolic acidosis)_ with normal respiratory compensation + **coexisting metabolic alkalosis** from vomiting. Hyponatremia, hyperkalemia and hypochloremia.

Answer 4

Fainting in the summer heat suggests **heat exhaustion.** The complaints and physical findings fit with severe dehydration. **Diagnosis: Hypernatremic Hypovolemia due to Heat Exhaustion** **Slightly low blood pressure** (normal is 120-130/80-85 mmHg) is sign o**f hypovolemia** **Hypernatremia** (normal is 135-145 mmol/l) A **common mistake** is that _sweat is hypertonic_ because it tastes salty, but it is **actually hyposmotic** because _most of the Na+ is reabsorbed in the sweat ducts._ And since the fluid lost is hyposmotic, the remaining fluid in the body will be hyperosmotic/hypernatremic. **Potassium is high-normal** (normal is 3.5-5 mmol/l): also indicates more fluid loss than electrolyte loss **Normal hematocrit** (f: 0.37–0.47, m: 0.40–0.54), **normal hemoglobin** (f: 120–165 g/l, m: 135–170 g/l): this rules out blood loss as a cause of for the hypovolemia **Microcytosis** (MCV normal is 80–95 fl) * **H2O is pulled out of the cells** by osmolar forces, leading to _cellular dehydration._ _Treatment:_ **Cooling** (remove from hot environment, ice packs near groin and axilla) Lay patient down supine or in **Trendelenburg position** _(feet elevated)_ to ensure perfusion to brain, prevent further fainting **Oral water replacement** (hypotonic fluid) o**r IV H2O (5% glucose solution)** if she’s still unconscious. * **5% glucose i**s an **isosmotic** solution which will **slowly restore balance**. Normal saline (0.9% NaCl) should not be used because the patient is hypernatremic.

Answer 5

Tubular damage: **Aminoglycosides** are known to be **toxic** to the **renal tubules** Weight gain **due to water retention** from **extremely low urine** output **Anuria** \< 200 mL urine / day 3 serum metabolite levels are **all elevated**, indicating **retention** due to **renal failure**: Elevated serum **creatinine:** (normal 40-130 µmol/L) Elevated serum **urea:** (normal 2 - 10 mmol/l) blood urea nitrogen **(BUN)** is ‘carbamid’ on the pathophys ref. ranges document) **Hyperkalemia**: (normal Se [K+] 3.5-5 mmol/L) _Diagnosis:_ **Acute Renal Failure (ARF)** due to **aminoglycoside toxicity**

Answer 6

**Tumor Lysis Syndrome** as a result of the **chemotherapy** fits best ---------------------------------------------------------------------------------------------------------------------------- Sodium is within normal range (135-145 mmol/l) The **high serum potassium** is a result of massive cell lysis from the chemo, which also causes the palpitations (normal is 3.5-5 mmol/l). We have too little information to fully explain the hypotension, but **probably from** either **arrhythmias** or from **cardiotoxicity** of the **chemotherapy** (normal BP is 120-130/80-85 mmHg) _**Low hematocrit**:_ **low RBC production** due to **bone marrow “overpopulation”** from the **malignancy,** and additionally from bone marrow **destruction from the chemotherapy** (normal htc for males is 0.40–0.54). Should **request HGB** (should be low) and **MCV(**should be microcytic) to **confirm** _anemia of chronic disease._ * *Disorientation** due to **low blood pressure** and **low blood supply** to the **brain.** - ---------------------------------------------------------------------------------------------------------------------------_What kind of **ECG-abnormalities** you expect to see?_ **Hyperkalemia** will change the T wave: **high amplitude** and **tent-like in most leads.** **QT interval** is **prolonged.** The QRS complex may be wider. This state is susceptible for **Vfib ("R on T").** * *Palpitations** are felt due to **arrhythmias** _from hyperkalemia_ - --------------------------------------------------------------------------------------------------------------------------- **_What would you do with him?_** **Dialysis** **Treat hyperkalemia:** * First and foremost we need to **stabilize the myocardium** using **IV Calcium-gluconate**, which antagonizes the hyperkalemia. * We can use **insulin** to activate the **Na+/K+ ATPase** and move the potassium intracellularly, also needs glucose to **prevent hypoglycemia** * When his _blood pressure and serum potassium levels normalize,_ we can start inducing **renal excretion of potassium** with a **thiazide** (inhibits Na+/Cl- antiporter) or **furosemide** (inhibits Na/2Cl/K symporter) diuretic. Treat **hypotension** and **low hematocrit:** * We need to **elevate the blood pressure** using **IV saline** (and maybe beta agonists?) * Hematocrit may be corrected with **blood transfusion** second this - **colloid IV is enough**

Answer 7

1. _Causes of direct hyperbilirubinemia:_ * **Infection** - hepatitis or any other infection can ↓ liver function * **Biliary atresia** - improper development of bile ducts * **Dubin-Johnson Syndrome** - AR mutation of canalicular MRP2 → ↓ hepatic excretion of bilirubin glucuronide (liver appears black) * **Rotor Syndrome** - AR mutation of OATP1B (organic anion transporting polypeptide) proteins for hepatic uptake of of bilirubin 2. _Causes of indirect hyperbilirubinemia:_ * **Physiological jaundice** - before birth glucuronyltransferase is downregulated in the fetus to keep bilirubin unconjugated and thus able to pass through the placenta and not accumulate in the fetus; it takes some time to fully function after birth b * **Erythroblastosis fetalis** - via Rh incompatibility → hemolysis * **Gilbert’s Disease** - low UDP-g transferase function, often asymptomatic unless stressed * **Crigler-Najjar** - 2 types: total or partial lack of UDP-glucuronosyl transferase * severe form can lead to kernicterus (bilirubin in brain) → brain damage * only treatment is liver transplant * phenobarbital can induce the enzyme in the less severe form * Phototherapy can be used to solubilize excess dermal bilirubin in neonatal jaundice.

Answer 8

_Clinical findings:_ **Rapid breathing** and less responsiveness cannot be explained from only this clinical anamnesis. _Laboratory findings:_ **[Na+**] is **lower** than **normal** (135-145mM), [K+] & [Cl-] are within normal ranges. * *pH** indicates **acidemia** - -------------------------------------------------------------------------------------------------------------------------- **aHCO3**- is **severely decreased,** indicating a **_metabolic acidosis._** --------------------------------------------------------------------------------------------------------------------------- * *pCO2** * *low,** probably **due to rapid breathing** as compensation. - -------------------------------------------------------------------------------------------------------------------------- **AG** (123 - (99 + 5)) = **19 mM,** is **higher than normal**, * indicates **_primary anion gap metabolic acidosis._** --------------------------------------------------------------------------------------------------------------------------- * *Expected pCO2** = * *13.5-17.5** the measured **value is les**s than this, * thus there is a **_coexisting respiratory alkalosis._** --------------------------------------------------------------------------------------------------------------------------- **Corrected HCO3**- = **12 mM,** * since **\< 22mM** there is an **_coexisting metabolic acidosis_**. --------------------------------------------------------------------------------------------------------------------------- **_Conclusion:_** This patient has **hyponatremia + primary anion gap metabolic acidosis** with **hyperventilation** making a coexisting **respiratory alkalosis**, and also coexisting **metabolic acidosis.** **Hyponatremia** can **explain** the **unresponsiveness** as it causes **confusion** and **lethargy;** **rapid breathing** due to **respiratory compensation** of acidosis. Addisons ? probably was an ecstasy overdose ( ONE LILAC AIRWAYS GUM PUH-LEASEEE)

Answer 9

- Pulmonary function test is **low** - Reversibility test: there is **improvements of FEV1 after salbutamol** (bronchial dilator): the obstruction is temporarily and reversible. Suggest **asthma.** - Key: allergy frequently precedes development of **asthma.** - FVC \> 80 % - FEV1: \> 80 % - Symptoms of **asthma**: chronic inflammatory disorder of the airways o Recurring episodes of **wheezing,** breathlessness, chest tightness, and coughing, particularity at night or in the early morning. Paroxysmal nocturnal dyspnea is due to respiratory depression during sleep worsening the already present pulmonary issues the minimum difference in % between FVC taken before and after Reversibility test to make a confident diagnosis of asthma. The answer is 15%. TYPES atopic, non-atopic, drug-induced and occupational asthma. _o Risk factors:_ house dust mites, animals with fur, pollens, respiratory (viral) infections, exercise, strong emotional expressions, chemical irritants, drugs (such as aspirin and beta blockers) etc.

Answer 10

* High ESR (\>20 mm/h) → inflammation * In inflammation, increased serum fibrinogen causes RBCs to stick together and form“rouleaux” which settle faster via increased density. * High WBC (\>10 G/l) indicates inflammation / immune reaction * High α-amylase (\>180 U/l), urine amylase and serum lipase indicates pancreatitis * Serum urea is borderline high → slightly impaired kidney function○ can be via redistribution of blood flow in early shock (low BP, high HR) * Creatinine is normal (40-130 uM) * Ca⁺⁺ is low (\<2.2 mM) indicating impaired fat digestion → ↓ vitamin D○ In pancreatitis, autodigestion via lipase → “saponification” of FFAs + Ca → ↓ Ca⁺⁺(elongated QT on ECG) * Serum albumin is low (\<35 g/l) indicating acute inflammation * Fasting glucose is high (\>6.0 mM) → low insulin secretion, but not actually… * ~90% islets must be destroyed before glucose ↑ * in acute inflammation, stress hormone elevation → high gluconeogenesis * Periumbilical or “belt-like” pain is typical of pancreatitis. * Low BP + tachycardia point to the beginnings of shock. * Shock Index = HR / Systolic BP … should be around 0.5-0.66 … \>1 indicates probableshock (means ↑ HR ↓ BP) * **This is acute pancreatitis** , because of the high ESR, low albumin and high serum/urine pancreaticenzymes. * Imaging studies (US, CT or MRI) can be done to confirm pancreatic enlargement * Commonly caused by cholelithiasis or alcohol and greasy foods. * Alcohol dehydrates pancreatic secretions + need for more lipase to digest foods →viscous secretions back up in pancreatic ducts → autolysis + inflammation * Treatment is symptomatic: NPO (“nil per os”, no food/drink by mouth) and painkillers (\*\*ESR: 42 mm/h. - suggesting inflammationWBC: 11 G/l - slightly elevatedserum α-amylase: 1800 U/l - highurine α-amylase: increasedserum lipase: increased\*\*\* acute pancreatitis (if lipase is not elevated the others could be a result of salivary glands)intense periumbilical pain of sudden onset - typical for acute pancreatitisserum urea: 10 mmol/l - slightly elevated (kidney failure due to shock)serum creatinine: 90 μmol/l serum Ca: 1.9 mmol/l (hypocalcemia - know the reason and the ECG sign)serum albumin: 30 g/l (low, maybe due to inflammatory reaction)fasting blood glucose: 6.5 mmol/l (any major inflammation/stress may cause)Acute pancreatitis.other tests: no need for further (amylase, lipase is enough)- other examinations are needed in order to check if the patient is getting better or worse (serum CRP - Everyday), which type of pancreatitis (adematus, necrotic) - imaging (US only size)(CT - will see necrotic area)\*\*)

Answer 11

* Weight loss, diarrhea/constipation + anemia in pt of this age → **GI malignancy** * Other possibilities for weight loss in elderly include depression , but with these GIsymptoms, tumor is likely * Alternating constipation + diarrhea due to **obstruction via tumor** → formation of large, dry stoolmass → osmotic activity of mass eventually draws a lot of water from bowel → diarrhea * Can perform an occult blood test - aka **“hemoccult”** test, recommended as yearly GI cancerscreening for pts above 45 * Can also check GI tumor markers : * **CEA** (carcinoembryonic antigen) - not specific, but often elevated incolorectal/gastric/pancreatic and other carcinomas * **CA 19-9** (carbohydrate antigen) - AKA Sialyl-Lewis A, elevated in colon/pancreaticcancers * Check hematocrit for the **anemia**: tumor may bleed directly or consume RBC co-factors * Perform endoscopy and colonoscopy. * Irrigoscopy - patient drinks contrast agent + GI tract is visualized; area where contrast not seenmay be tumor * Can do various imaging studies (MRI, CT, etc.) for metastases (\*\*Colon cancer constipation alternating diarrhea is due to blockage in the GI, build up of . .. + bacteria will digest and thats why diarrhea.Check for blood in ... Colonoscopy - to see the inside, if suspecting in the microscopy, biopsy is takenCT examination gives s good idea but no biopsy can be taken.\*\*)

Answer 12

It is normal to lose kidney function with age, and with this patient **being “elderly”,** we can assume a **reduced GFR.** It can be as low as 40-60 ml/min (normal is 120 ml/min) **Beer is a hypotonic** solution with some alcohol, and **max recommended fluid intake** is **1.2 L/hour** in _healthy_ adults, _less in elderly_ (kidney excretion rate). The patient has drunk **2 L/hour,** which resulted in **_water poisoning (hyponatremic hypervolemia),_** especially with the reduced GFR. Acute water poisoning with _se[Na+] \> 120 mmol/l_ leads to **brain edema.** This seems to already have started in this man, considering complaints and **plantar extensor/Babinski reflex** (sign of _increased intracranial pressure_). **BP is high** (normal 120-130/80-85 mmHg) is because of **hypervolemia.** [Na+] is reaching critically low levels (normal is 135-145 mmol/l) . We should expect hyperkalemia because of the decreased kidney function, however it might be masked by dilution (normal is 3.5-5 mmol/l). He has **macrocytic RBCs** because the osmolar forces are pulling water into the cells (normal MCV is 80–95 fl) **Hematocrit** appears **low** because of **dilution** by the **hypervolemia**, this is most probably not anemia (normal htc is 0.40–0.54 in males) High _serum creatinine_ and _urea_ levels **(azotemia) indicate renal failure.** (normal cr is 40–130, normal urea is 3.5–7.0) His urine **density** is within the **normal range** (1.010–1.035), however, with water poisoning we **should expect a lower urine density**, closer to water, so his density being in the normal range actually **indicates insufficient kidney** function, he **cannot dilute** his urine enough. **Increased sodium** in the **urine** is another sign of **insufficient kidney** function (normal is \<20 mmol/l). **_Diagnosis:_** A healthy person would probably have been able to handle this amount of fluid/alcohol, however, **as you get older your kidney function decreases,** resulting in a markedly **reduced GFR.** This patient suffers from **_water poisoning from drinking too much_** and having age-related renal failure. **_Treatment:_ IV Mannitol** (a non-metabolizable osmotically active solution that will pull water out of his cells). He may also need dialysis.

Answer 13

Probable Cause: **Hypovolemic Hyponatremia** due to **renal failure** and **diarrhea** Diarrhea → hypovolemia →general sympathetic redistribution of blood→hypoperfusion of kidney→low GFR → release of renin → angiotensin II → more constriction in afferent arteriole of glomerulus NSAID comes into play→ no PGE → not only afferent, also vasa recta constriction → **medullary hypoxia** → tubular lesions → **no reabsorbtion** of **Na+** and excretion of **K+.** This effect is called **analgesic nephropathy** or **phenacetin nephropathy** The kidney failure explains increased sodium excretion and potassium retention. The **diarrhea** is a **cause of dehydratio**n that can also worsen the electrolyte abnormalities. **Orthostatic hypotension** due to **hypovolemia.** Explains dizziness, needing to sit down. (normal BP is 120-130/80-85 mmHg) **Hyponatremia**: related to **high urinary sodium excretion** (normal is 135-145 mmol/l) **High urinary sodium:** a sign of **renal failure,** inability to perform normal sodium reabsorption (normal is \<20 mmol/l) **Hyperkalemia**: normal for renal failure due to **decreased urinary excretion of K+** (normal is 3.5-5 mmol/l) **High hematocrit:** due to **hypovolemia** (normal is 0.37–0.47 for females) High serum creatinine and urea **(azotemia):** indicates **renal failure** (normal cr is 40–130, normal urea is 3.5–7.0) Note that overdose of **NSAIDS also causes acute tubular necrosis (ATN)** **Decreased skin turgor**: when pulled, the skin takes an **abnormally long time to return** back to normal shape. This is a typical **sign of dehydration.**

Answer 14

* indirect bilirubin is high; direct is normal indicating increased hemolysis with normal UDP-glucuronyl transferase function * ASAT/ALAT are normal indicating no liver damage * Urine bilirubin is absent (only conjugated bilirubin enters urine) * LDH is high indicating hemolysis (specifically **LDH1** from RBCs) * Ht is low (\<0.37 l/l) indicating anemia/hemolysis * Haptoglobin/hemoplexin are proteins which bind broken down Hb in the blood, ↓ indicates intravascular hemolysis * So the cause of jaundice is **intravascular hemolysis** , but the cause of hemolysis is unknown and must be determined. * Can check for viral / autoimmune (RA/SLE) / allergic (penicillin) / etc. causes

Answer 15

**Low urine volume** (normal: 1-1.5L/day) Considered **oliguria** because it’s between 200 and 500 mL/day. Below 200 mL is considered anuria. +++ = **Large proteinuria** (normal is 50-150 mg/day. Pathological if \> 300mg/day. Considered “massive proteinuria” if \> 3 g/day) Causes **edema** from the **reduced** capillary **colloid osmotic pressure** Sediment shows **hematuria /** significant red blood cells in the urine (considered microscopic hematuria is **\>3 RBCs per high power field**) **Very Low GFR** (normal creatinine clearance is 120-125 mL/min) Kidneys are failing to properly filter the blood, probably due to glomerular inflammation **Low GFR ⇨ water retention ⇨ hypertension**, both of which also contribute to edema _Diagnosis:_ **Nephritic Syndrome** based on **hematuria** (if it was only protein and no blood, then it would be nephrotic syndrome) Probably due to **post-streptococcal glomerulonephritis** (upper respiratory infection, then weeks later ⇨ glomerulonephritis with **immune complex deposition in glomeruli,** between the basement membrane and podocytes. Immune complexes activate the complement system, causing **inflammation** and **damage** to the **filtration barrier,** allowing proteins to leak into the urine)

Answer 16

**Dyspnea** and **cyanosis** is indicative for **respiratory failure**, which could be **hypoxia** (pO2 \<60 mmHg) or **hypercapnia** (pCO2 \>50 mmHg). As you can see on the lab values, **this respiratory failure** is caused by **hypoxia,** thus a **hypoxic respiratory failure (type I).** Productive cough and **feve**r indicates an **infection,** this in combination with **low BP,** **high HR** and **high resp. rate** points towards a **septic shock.** Lung sounds can indicate that lower lobes are mostly affected and that the hyperventilation involves the upper lobes. ----------------------------------------------------------------------------------------------------------------------------- _ABG results:_ **_pH_** is in the **upper range of normal**, but not alkalemia, can however argue that it is the start of an alkalosis (alkalizing process in the body). ----------------------------------------------------------------------------------------------------------------------------- **_pCO2_** is lower than the normal range (35-45 mmHg), which **will increase the pH**. * Can be explained by the **high resp. Rate.** ---------------------------------------------------------------------------------------------------------------------------**_pO2_** is at **hypoxic** levels (n: 80-105 mmHg), which could be explained by a **pneumonia/sepsis** → inflammation →**pulmonary edema.** Due to the **lower diffusion potential** of **O2** compared to **CO2** (20 times lower), **pO2 decreases more** than pCO2 increases. The patient experience an **increased ventilatory drive**, but in the attempt to normalize the pO2 → **hyperventilation** → **decrease pCO2** → **respiratory alkalosis.** ---------------------------------------------------------------------------------------------------------------------------**_aHCO3-_** is lower than normal (21-26 mM), which would decrease the pH, thus indicative of metabolic acidosis. -----------------------------------------------------------------------------------------------------------------------------**_stHCO3-_** is only slightly lower than normal. -----------------------------------------------------------------------------------------------------------------------------**_AG_** is normal (10-14 mM), which means there are no additional anions not accounted for → “non-AG” or “hyperchloremic acidosis” ----------------------------------------------------------------------------------------------------------------------------- **Expected pCO2** **= 33-37,** measured **value is much lower** indicating an additional **respiratory alkalosis.** **Corrected HCO3**- = **18 mM,** so there is an **additional metabolic acidosis.** (Corrected HCO3- is calculated with the following formula, and if **\< 22 mM i**ndicates an **additional metabolic acidosis:** (Corrected HCO3- = aHCO3- + (AG - 12) ) ----------------------------------------------------------------------------------------------------------------------------- Conclusion: **Hypoxic respiratory failure** due to **pulmonary edem**a caused by **pneumonia** or **sepsis** (pt. fulfills 3 of the SIRS criteria, with leukocytosis being unknown). As there is **hyperventilation** we can see the start of a **primary respiratory alkalosis,** with **coexisting metabolic acidosis.** ---------------------------------------------------------------------------------------------------------------------------- _What other test would you order to verify your diagnosis?_ **Chest x-ray** - confirm **pneumonia** **Culture** - to identify **causative agent** →targeted therapy **Blood work** - to check **ESR**, **a**cute **p**hase **p**roteins (e.g.: CRP), **WBC count**

Answer 17

Middle-aged woman, hardening skin and fissures could be CREST/Scleroderma[1] Progressively worse exertional dyspnoea could be anything, but fits with Scleroderma CXR shows **bilateral opacification** of the bases of the lungs which is indicative of **interstitial lung disease** The **RVH** is due to **pulmonary hypertension** caused by the **chronic pulmonary fibrosis** Pulmonary Function tests show decreased FVC, FEV1 and increased TI FEV1 ≤ 80%, FVC ≤ 80% and TI ≥ 70% is indicative of **restrictive disease** This fits with **scleroderma** **TLCO** (Transfer factor of the Lung for CO) is aka DLCO (Diffusion lung capacity for CO). **(normal is 81-140%)** This is the result of a Gas Transfer Test, using CO because it has a similar diffusion capacity to O2. **TLCO** is **decreased** in **any condition** which affects the **effective alveolar surface area**, this patient’s decreased TLCO fits with Scleroderma **KLCO** (TLCO corrected for alveolar volume) **should be lower than TLCO**. A **KLCO** that is **higher** than **TLCO** indicates that the **restriction is extrapulmonary.** In this this patient the KLCO is lower than TLCO disproves extrapulmonary restriction (obesity, kyphoscoliosis, ascites) _ABG:_ **paO2** is decreased in rest. Exercise shows that compensation to strain is insufficient. **paCO2** decreasing below normal values (35-45 mmHg) shows that she is **hyperventilating.** CO2 has a much higher diffusion capacity than O2, because of the pressure-gradient, and so is **easily “excreted”** even though she has a reduced alveolar volume. However O2 hit its diffusion capacity even before exercise (she was hypoxemic at rest), and **paO2** continues to **decrease.** **ECG:** RV strain due to hypoxia, **p pulmonale** due to **pulmonary HTN,** which again, is caused by the **pulmonary fibrosis** Dx:Pulmonary tests, ABG and ECG point to **Interstitial Lung Disease,** which could be explained by **systemic scleroderma (**Autoimmune hyperproduction of Collagen[2] ). Check autoantibodies to confirm (local form has anticentromeric Ab, diffuse has **anti-topoisomerase Ab**) also **anti-RNAP 3** Systemic Scleroderma reaching the lungs indicates a 70% 5-year survival There is **no cure, h**owever it was mentioned that you can treat/ alleviate symptoms with anti-fibrotic drugs and immunosuppressants. CREST refers to limited scleroderma, just from the fact that there is hardening of skin cant exclude it. But because of the lung involvement this is **systemic (diffuse) scleroderma.** autoimmune disease leading to fibroblast overactivation -\> overproduction of collagen

Answer 18

Calculated TI = 62% Semi-old man, buckets of sputum, 80 pack years. High risk of COPD, symptoms of **Chronic Bronchitis** **Cyanosis,** prolonged exhalation and wheezing **fit with obstructive disease** Should check **chest diameter,** patients with **Chronic Bronchitis** can have a **“barrel chest”** (barrel chest + cyanosis → **“Blue Bloater”** chronic bronchitis phenotype) - In this case he has **increased amount of sputum**: looks like an **acute upper respiratory inflammation** - Suggest **obstructive lung disease:** blue bloater? - pO2: low - pCO2: not so high, should be high in chronic bronchitis. - There is an **acute worsening** of the condition: **probably hyperventilation**, that brings pCO2 back to near normal. - Pulmonary function test: **very bad** o **FVC** and **FEV1**: is **very low** o TLC and RV: is increased o RAW: resistance of airways: probably low. - Reversibility test: **no difference**, which means it is not asthma. - Ventillatory defect: obstructive disease **- Chronic bronchitis, with acute worsening of the condition.** **- Chronic bronchitis** Raw = Rairway isn’t really mentioned elsewhere, but Hamar says we only need to know that it is an abbreviation for airway resistance, and it's increased because of the obstruction. **Salbutamol-test** shows 2% and 1% increase in FVC and FEV1, **disproving asthma** Diagnosis: **Severe COPD** o Chronic cough associated with sputum production more than 90 days on 2 successive years. o Cause: Smoking, air pollution, occupational exposure, etc.

Answer 19

* High bilirubin + urine bilirubin → hyperbilirubinemia , of conjugated type b/c only conjugated gets to urine * Ubg decrease → obstruction , no bilirubin to GI tract * ASAT is slightly increased → mild liver damage * ALP is very high (\>150 U/l) → obstruction * GGT is high (\>60 U/l) → obstruction * Obstructive jaundice has two common possible causes: **malignancy or cholelithiasis** * In a young (30 yr old) and overweight (81 kg @ 164 cm) patient, **gallstones are the most likely cause** * Perform abdominal **ultrasound**.