1 semester II Flashcards

Question

3. A **febrile** patient complains of **lumbar** pain. _Urinalysis:_ protein: ++ pus: **+++** sediment: a lot of **leukocytes**, some **erythrocytes**, epithelial cells, **a lot of bacteria, leukocyte casts** C_K: 100 ml/min ESR: **38 mm/h** What is the presumable diagnosis?

Answer 1

Moderate protein in urine: (normal \< 300 mg/day / day). Some **glomerular damage** **Pyuria:** pus in urine, **sign of urinary tract infection (E.coli , enterofaecalis)** **Leukocytes** in urine indicates **infection**, while **RBCs** and **epithelial cells** indicate **damage** **Leukocyte casts** indicate **pyelonephritis,** as they are made in the tubular system. Slightly Low C_K: some **impaired kidney function** **Increased ESR**: (normal is \< 20 mm/hour) ESR normally is **increased with inflammation** due to **acute phase protein synthesis**, specifically that the **increased serum fibrinogen** causes **RBCs to clump t**ogether and settle at a faster rate. _Diagnosis:_ **Pyelonephritis.** Pyelonephritis usually is the result of **ascending urinary tract infection. Lumbar pain** occurs **due to inflammation** distending the renal capsule, and **fever** occurs due to organ infection stimulating **systemic cytokine responses.** _Examples include_ albumin,[5] transferrin,[5] transthyretin,[5] retinol binding protein, antithrombin, transcortin. The **decrease** of such proteins may be **used as markers of inflammation**. The physiological role of decreased synthesis of such proteins is generally to save amino acids for producing "positive" acute phase proteins more efficiently. Theoretically, a decrease in transferrin could additionally be decreased by an upregulation of transferrin receptors, but the latter does not appear to change with inflammation.

Answer 2

_Diagnosis:_ Mild **Urinary Tract Bleeding,** probably from **kidney stone** (nephrolithiasis) Slight **Microscopic Hematuria:** normal is \< 3 erythrocytes / HPF Normal Morphology **(Isomorphic) RBCs**: indicates the **bleeding** occurs more **distally** in **the urinary tract** If there is **glomerular damage** where red blood cells enter the tubules for filtration, then the cells are present during the concentrating process, which **dehydrates** them ⇨ **small, dysmorphic erythrocytes**. That did not occur here, so the glomeruli and tubules are probably fine. **Minimal proteinuria**: the equipment is not sensitive enough to show proteinuria \< 300 mg / day : also suggest that it is not a glomerular bleeding, always goes together with a significant proteinuria **“No selectivity in the proteinuria**”: since bleeding is likely distal in the urinary tract, no filtration barrier is involved**. Blood l**eaks **into** the **urine,** and so **all proteins can get in.** Normal Creatinine Clearance: **GFR is not impaired**

Answer 3

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 4

- If the **GFR is decreased** enough, the **glucose load** is also **decreased**. Normally, glucose is reabsorbed in the tubules up until it reaches the BGL concentration of **10 mmol/L**, at which point the **SGLT transporters are saturated** In this case, the **GFR is so low** that **glucose has time** to be **reabsorbed** in the **tubules by SGLT2** transporters, which are not damaged * **Less glucose** per time is **filtered** into the renal tubules. This gives the patient _more time to reabsorb the glucos_e. Thus, glucosuria will not develop. - If the GFR is very low, the patient will have a higher tubular threshold and the glucose will not be detected in the urine. - ------------------------------------------------------------------------------------------------------------------------- - **Tubular function test: negative** o **Measure: beta-2 microglobulin is elevated:** show tubular dysfunction -------------------------------------------------------------------------------------------------------------------------- _-**Concentration + dilution test:** follow up!_ **Concentration** test: dinner without fluid and no drinking of fluid throughout the night: urine in the morning is analyzed for its density. If the urine in morning is not concentrated, it means that something wrong. It should be increased. * *Dilution** test: drink 1-2 L tea or a large amount of fluid; then the urine sample should have low-density values, and low osmotic cc.→ If the urine is not diluted, so it does not go below 1,010 kg/l (density→ there is a problem with dilution of the urine - ------------------------------------------------------------------------------------------------------------------------- - Patient wit**h chronic renal disease** loose first the **concentration capability** and later they loose the **dilution capability** (end stage: cannot concentrate nor dilute – the urine osmolarity is the same as the urine – called isostenuria.

Answer 5

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 6

**Actual HCO3-** - directly measured bicarbonate of the blood sample **_Generation_**: aHCO3- is dependent on both metabolism and respiration. In **respiratory acidosis** (not breathing sufficiently) **pCO2 increases**, and due to _Le Chatelier's principle_ **more** **HCO3- is formed.** CO2 + H2O ←→ H2CO3 ←→ **HCO3- +** H+ (shifts rightward) **_Compensation:_** Th**e kidney** compensates by **reabsorbing more HCO3-** (in the proximal tubule) and **secreting H+** in the form of **NH4+** (in the distal convoluted tubule), thus as compensation goes on more HCO3- accumulates in plasma. ---------------------------------------------------------------------------------------------------------------------------- **Standard HCO3-** **_Generation:_** stHCO3- is **only dependent on metabolism,** because the value is measured after equilibrating the sample to 40 mmHg pCO2. There is initially no metabolic change (compensation), and thus no change in the value. **_Compensation:_** However, **after** the increase in **HCO3- reabsorption** we can see an **increase** in **stHCO3-.** ---------------------------------------------------------------------------------------------------------------------------- **Base excess (BE)** **_Generation:_** this value shows base deficit r**eflecting the metabolic side**, and initially there is no change in the metabolic side. **_Compensation:_** as explained above there will be an increase of HCO3- (base) due to kidney compensation, thus **BE will show a positive value** (pos. = base excess/lack of acids). ---------------------------------------------------------------------------------------------------------------------------- Note that **compensation** by the **kidney** takes maybe **6-8 hours** before working, and up to 3-5 days before maximal effect. This is **because synthesis** of **channel proteins** in the kidney is needed **for the compensation.**

Answer 7

_During first hours_ **pH** indicates **acidemia** (normal is 7.35-7.45) **HCO3**- indicates of metabolic origin (normal is 24 mmol/L) AG cannot be determined. Cannot calculate corrected HCO3- without AG. **pCO2** is **low** (normal 35-45 mmHg), but expected pCO2 = 18-22 mmHg according to Winter’s formula (below). * pCO2 measured is within this range, thus compensation is normal. * Winter’s formula is used to calculate the expected pCO2 in respiratory compensation of an acid-base disorder, and its results are sometimes approximated as **pCO2 ≈ last 2 digits of pH**: pCO2 = (1.5 x HCO3-) + 8 +/- 2 **BB** is **low** (normal 45-52 mmol/L) because bases in blood are used up as buffers. **BE** is **strongly negative** (normal 0 +/- 2.5 mmol/L) - lack of base, excess of acids _Conclusion:_ **Primary metabolic acidosis** with **normal** _respiratory compensation_. _One day later_ **pH i**ndicates **acidemia** Both **pCO2** & **HCO3**- indicates **acidosis** **Expected pCO2** = **25.5-29.5**, * pCO2 measured is higher than the expected value, thus there is a **coexisting respiratory acidosis**. \>50 mmHg -\> **hyperkapnia.** No change in BB or st.HCO3- can indicate lack of kidney compensation? (just something I believe)[1] [2] [3] [4] [5] _Conclusion:_ the **original metabolic acidosis** has **worsened** due to **inadequate lung compensation** because of **ARDS** (referred to as “shock lung” in the question). - --------------------------------------------------------------------------------------------------------------------------- * *Metabolic acidosis + respiratory acidosis** - ---------------------------------------------------------------------------------------------------------------------------

Answer 8

**- Diabetic ketoacidosis:** Diabetic ketoacidosis (DKA) is a **potentially life-threatening** complication in patients with diabetes mellitus. It happens **predominantly** in those with **type 1 diabetes,** but it can occur in those with type 2 diabetes under certain circumstances. - DKA **results from a shortage of insulin**; in response the body switches to burning fatty acids and **producing acidic ketone** **bodies** that **cause most of the symptoms** and complications. --------------------------------------------------------------------------------------------------------------------- **pH,** will **decrease** because of **ketones** (acetoacetic acid & beta-hydroxybutyric acid), but as **compensatory mechanisms** start to **work** it will **become less acidic**. However, if the DKA is not treated, more ketone bodies are produced and thus acidosis will worsen. --------------------------------------------------------------------------------------------------------------------- **pCO2,** changes in pCO2 are related to compensation, so **initially there is no change**. As **ventilation** is **increased** to decrease H+, **pCO2 will decrease**. * Patients with DKA typically present with **Kussmaul breathing** pattern (rapid & deep). --------------------------------------------------------------------------------------------------------------------- **_BE_** will be **strongly negative** **(acid excess / lack of base)**, but when the kidney starts compensating there will be an increase of HCO3- and thus a bit less negative value --------------------------------------------------------------------------------------------------------------------- * *_aHCO3_** * *-**as there is an increase of H+, **HCO3- will be depleted as a buffer.** As **pCO2 decreases** via lung compensation, **aHCO3- will decrease further** (again via Le Chatelier, the ↓ pCO2 shifts the carbonic anhydrase equation away from bicarb production). * **As HCO3- is reabsorbed**, because of **kidney compensation** there is a **slight increase** in its serum concentration. --------------------------------------------------------------------------------------------------------------------- **_st HCO3_** –will also be depleted as a buffer, is not affected by the lung compensation, and is also increased due to kidney reabsorption. --------------------------------------------------------------------------------------------------------------------- **_AG_** high due to increased amount of anions (ketones) not accounted for in the formula. --------------------------------------------------------------------------------------------------------------------- _**se K+**,_ increased: **Insulin** is a **stimulator** of the **Na+/K+-ATPase**, thus **lack of insulin** will lead to **decreased cellular uptake**. Note that from this mechanism there is **not an increase** in the **total** body **potassium,** **just** a change **in its distribution.** Most **somatic** cells have a **H+/K+-exchanger,** in acidosis there is a tendency for **cells** to use this to **take up H+** and **excrete K+**, also resulting in movement of potassium extra cellularly.

Answer 9

**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 10

**RA** can be treated with **aspirin** as in this case, as a **side effect** it can **induce nausea** and **vomiting**. **Vomiting** causes **loss of H+**, thus **increasing pH.** 3-5 pills/day indicate aspirin overdose (NOT SURE WHAT THE LIMIT IS) _ABG results:_ **pH** indicates **alkalemia** **pCO2** is **lower than normal,** thus **increasing pH**. * Aspirin **overdose** triggers **rapid** and **deep** **breathing.** **aHCO3-** is **higher than normal**, thus **increasing pH.** Due to l**oss of H**+ by **vomiting.** **AG** is **22 mM,** if **AG \> 20 mM** then there is a **primary metabolic acidosis** _regardless of pH or HCO3-._ As aspirin is an acid not accounted for in the AG formula it is probably the causes of the gap. **Expected pCO2** is **51-55,** the measured **value is lower** than this, thus pt. has an **additional respiratory alkalosis.** * *Corrected HCO3 - **is**40 mM**, because**\> 26mM**there is an**additional metabolic alkalosis.** _Conclusion:_ This is a complex picture caused by **aspirin overdose**, AKA **“salicylate poisoning”:** Triggers **nausea** and **vomiting,** thus **loss of H+** (additional metabolic alkalosis) Triggers **rapid** and deep **breathing** and thus a **respiratory alkalosis.** Aspirin in **it self is an acid**, thus causing the **high anion gap** and **primary metabolic acidosis.** So **primary metabolic acidosis** with co-existing **respiratory** and **metabolic alkalosis.**

Answer 11

_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 12

_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 13

_Clinical findings:_ **Patients** receiving **BM transplants** are **immunocompromised**, thus infections are common and normally **“innocent” infections** can become **life threatening**. Antibiotics is given for bacterial- and **amphotericin B** for **fungal infections**. Some antibiotics have side effects, for example being **nephrotoxic** (e.g.: amphotericin, aminoglycosides) possible causing **_ARF from tubular toxicity._** Rigors are typical for electrolyte disturbances. **Dyspnea** has many causes, but here seems to be due to a **respiratory infection** being **treated** with antibiotics and **amphotericin B..** _Laboratory findings:_ * *[Na+]** is **low** (n:135-145mM), * *[K+]** is **low** (n:3,5-5,0 mM), * *[Cl-]** is **normal** (n:95-105 mM) **pH** is severely low, indicating **acidemia**. **aHCO3**- is also severely low, indicating a **_primary metabolic acidosis_**. **pCO2** is low, indicating **_respiratory compensation._** **AG** (125 - (100+8)) = **17, _anion gap metabolic acidosis_** **Expected pCO2** = **18-22** mmHg, measured **pCO2 is higher** than this, thus there is a **coexisting respiratory acidosis**, likely due to a **respiratory infection** causing **dyspnea** + i_nsufficient compensation_ of the primary acidosis. **Corrected HCO3-** = **13** mM, since **\< 22mM** there is an additional metabolic acidosis. _Conclusion:_ **Primary anion gap metabolic acidosis** with coexisting **respiratory** - and **metabolic acidosis.** **Rigors** can be explained **by hypokalemia**, or simply by **chills** and **fever** associated with **infection.**

Answer 14

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 15

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 16

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 17

**DKA** is an acidosis caused by the presence of **excessive ketoacids** produced because of the body’s **inability to use glucose**. It usually occurs as a consequence of absolute or relative i**nsulin deficiency** that is accompanied by an increase in counterregulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). DKA is **treated with fluids, electrolytes** — such as sodium, potassium and chloride — and insulin. Perhaps surprisingly, the **most common complications** of diabetic ketoacidosis are **related to this lifesaving treatment.** _**Total potassium** of the body_ Potassium exists **mostly in the IC** compartments of the body **(97%),** however, in an **acidemia** the potassium is **exchanged for protons,** and **pulled out** of the cells. Additionally there is probably a **hyperkalemia** (explained below), which means that there is more potassium to be lost. Then, a lot of this serum potassium is **lost into the urine because of osmotic diuresis,** remember that the pumps in the tubules reabsorbing electrolytes not only rely on concentration gradients, but _also charge gradients._ For these reasons, **Total Potassium of the body is decreased** _**Total sodium** of the body_ Sodium exists **mostly in the EC** compartments of the body **(90%)** Thus we expect **massive sodium loss** due to **osmotic diuresis**, way past the kidney’s ability to reabsorb _Total water (fluid) of the body_ Around ⅔ of our water is IC, ⅓ is EC. **Massive water loss** due to **osmotic diuresis**, **ketones** and **glucose** have a huge **osmotic pull,** and will _pull the water out of the cells,_ the kidneys won’t be able to keep up, and it will **be lost in the urine.** We expect cellular dehydration and microcytosis (MCV \> 80 fl) Does the serum potassium concentration change in parallel with the total potassium amount of the body? No, they do not change in parallel. This is explained by three events: Firstly, water loss is greater than potassium loss, and so hyperkalemia develops. Secondly, the kidneys are trying to combat the acidemia by extracting protons from the serum, in exchange for potassium (H+/K+ exchanger), and so hyperkalemia develops Thirdly, absence of **insulin** means that the **Na+/K+ ATPase is inadequately** stimulated, and so **more K+ is left in the serum** and not retained intracellularly. * This is important to keep in mind for treatment, when insulin is given it will rapidly deplete the extracellular potassium, causing a transient hypokalemia. ---------------------------------------------------------------------------------------------------------------------------- **How do you think the appropriate treatment will change the serum potassium concentration?** Tx of DKA: **Dialysis:** This case is very severe, we need to work fast **Calcium-gluconate** to **antagonize the hyperkalemia** in the cardiomyocytes and **prevent fibrillations** (Calcium-gluconate *_prevents K+ from entering the cardiomyocytes,_* without affecting serum K+-levels) **Insulin** Lack of insulin is the cause of DKA. Insulin draws glucose into the cells, **correcting** both the **hyperglycemia** and the **cell starvation** that causes ketone production/acidosis. We also need to **observe glucose-levels** to **prevent** insulin-induced **hypoglycemia** Insulin will **restore the Na+/K+ ATPase activity**, pumping K into the cells and removing it from the extracellular space. Additionally, the total body potassium is reduced due to the osmotic diuresis. Thus, **hypokalemia can rapidly develop** as fluids are replaced and insulin stimulates the Na+/K+ ATPase. (note the main risk of hypokalemia is **respiratory muscle paralysis)** Correction of fluid loss with **intravenous fluids** (Lactated Ringers solution) Slow, or i**ntermittent infusion of K+** will almost certainly need to be used, monitoring K+-levels during the treatment is extremely important Correction of acid-base balance with bicarbonate This treatment is extremely complex due to the intricacies of the body’s own homeostatic systems. P**otassium is one of the primary issues**, as its concentration in the serum **needs to be kept within a very narrow range due to arrhythmias** etc. According to the department, the preferred order of treatment is first **fluid + electrolytes** (via lactated Ringer’s), then **insulin** (slowly), then **K+**

Answer 18

**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 19

**Her blood pressure is low** (normal is 120-130/80-85 mmHg) and she is **tachycardic** (normal HR is 60-100) Patient had **circulatory shock** due to the **trauma** with likely significant internal hemorrhage. There is **high risk of MOF** (Multi-Organ Failure), with *significant renal damage.* _The emergency treatment is the following:_ **Stop** any **bleedings** etc (ABC) Restore the **blood pressure** with **IV Dextran dialysis, calcium-gluconate and insulin** (Unsure whether starting dialysis is part of the emergency treatment, but you would definitely start dialysis immediately when you see her labs) _How can you explain the parameters seen later?_ From the lab values we can tell that her **potassium is way too high** (normal is 3.5-5), we need to **stabilize her heart with Calcium-gluconate,** and move potassium into her cells with **insulin.** When giving insulin you need to be _wary of hypoglycemia._ Her lab values are **all signs** of **acute kidney failure**: **Oliguria** (on borderline of anuria, which is \< 200 mL/day) (normal is 1-1.5 L) * Her urine output should be increased, give IV Mannitol, and continue dialysis **Elevated sodium** (normal is 135-145 mmol/l) - can be explained by **renal hypoperfusion** → decreased GFR → RAAS → Aldosterone action to try and increase blood pressure. **Elevated potassium** because of **trauma/necrosis** and also **kidney failure** (normal is 3.5-5 mmol/l) Elevated serum creatinine and urea **(azotemia)** (normal cr is 40–130, normal urea is 3.5–7.0) is a clear **sign of acute renal failure .**Kidneys get so little blood that **kidney cells can die →** oliguria. Usually **tubular cells** die in case of **anoxia → Acute tubular necrosis.** **Hematocrit is low** because of the **bleeding** from the **trauma, t**hat has not been corrected by a blood transfusion (normal for females is 0.37–0.47)[2] _Retention parameters:_ **all are increased →** sugges**t renal insufficency** **Kidney regenerate:** can become healthy, depending on the extent of the renal damage. If **function does not** come back, **transplantation** is needed, this is better than chronic dialysis. _Emergency treatment:_ o **Fluid replacement :IV DEXTRAN** increase renal blood flow o Ultrasound: check organs o **Oxygen** o Pain killers o antibiotics