2 Flashcards
A 69 yr old came with confusion. He had nausea, vomiting, back pain. His serum calcium level is 14.1mg/dL
What’s the most appropriate next step?
Long term Rx
IV hydration with NS to restore IV volume n promote urinary Ca excretion. + calcitonin (inhibits osteoclasts mediated bone resorption)
Long term Rx- bisphosphonates
Emergent Rx of hyperkalemia is indicated if (3 indications)
Emergent Rx is with?
Then slow acting (removal of k from the body) is with?
- Rapidly rising serum K+
- K+>6.5
- EKG changes
Iv calcium gluconate or CaChloride,b2 adrenergic agonists, insulin with glucose
Hemodialysis, cation exchange resins, diuretics
A 57 yr old HIV pt developed chest infection n started on ceftriaxone, azithromycin, trimethoprim- sulfamethoxazole, albuterol
On the third day his k+ is 5.9 n creatinine is 1.5
Which of the above meds is responsible?
Trimetoprim- it blocks the epithelial sodium channel in the collecting tubules similar to amiloride, a k+ sparing diuretic
It can also cause an artificial increase in creatinine by blocking its secretion
A 71yr old man with hypernatremia came with decreased mentation. BP-90/60, PR- 98, dry oral mucosa
Most appropriate next step in the mx?
Different mx options based on hydration status
IV 0.9% saline since the pt has severe hypovolemia
Mild cases can b treated with 5% dextrose in 45% saline and euvolemic/hypervolemic hypernatremia can b treated with 5%dextrose in water
Nephropathies secondary to 1.DM
2. Htn r cxd by?
- DM- increased extracellular matrix, basement mem thickening, mesangial expansion, and fibrosis
- Htn- arteriolosclerotic lesions of afferent n efferent arterioles n glomerular capillary tufts
In a normotensive pt with hypokalemia n met alkalosis
What r the 4 ddx? What’s the place of urinary chloride concentration in differentiating one from the rest?
1. Surreptitious vomiting- low urine chloride. The rest- high urine Cl - diuretic abuse - bartter syndrome - gitelman’s syndrome
Rapid correction of hyponatremia and hypernatremia would each cause?
Hyponatremia- osmotic demyelination/ central pontine myelinolysis
Hypernatremia- cerebral edema
A 47yr old female came with lower abdominal pain that is relieved with voiding for over 2 months. She also has frequency n dyspareunia. On p/E no cervical motion tenderness, palpating the anterior vaginal wall elicits severe pain. U/A is normal. Most likely Dx?
The disease is commonly associated with?
Clinical presentation?
Painful bladder syndrome (interstitial cystitis)
Associated with anxiety, fibromyalgia…
Bladder pain with filling n relief with voiding, frequency, dyspareunia
Difference between IgA nephropathy n Postinfectious GN
- onset after URTI
- complement levels, kidney biopsy
IgA- within 5 days of URTI - normal complement - mesangial IgA deposits seen PSGN- 10-21 days - low C3, - subepithelial humps consisting of C3
- Normal PH, HCO3, PaCO2 range
- Normal anion gap, AG formula
- 6 most common causes of anion gap metabolic acidosis
- PH - 7.35-7.45; HCO3- 22-28; PaCO2- 33-45 mm hg
- AG= 6-12
AG=Na-(HCO3 + Cl) - Lactic acidosis; Ketoacidoais; uremia, toxic alcohol(methanol) ingestion; salicylate toxicity; ethylene glycol ingestion
How does vomiting cause metabolic alkalosis, generation n maintenance phases? Initial Rx for such pts?
Generation- acid is lost thru the vomitus along with
Na,Cl,K. —> bicarb accumulation (Normally gastric acid is responsible for stimulating the pancreas to secrete(excretion) HCO3 ) —> met alkalosis.
Maintenance- loss of fluid—> RAAS—> contraction alkalosis
Rx- iv NS( stops RAAS activation), K+ supplement
Associated conditions with
- Minimal change dis
- Membranous nephropathy
- Membranoproliferative GN
- FSGS
- NSAIDs, lymphoma
- Adenocarcinoma, NSAIDs, SLE, Hep B
- HepB n C, lipodystrophy
- HIV, heroin use, obesity
The most common form of nephrotic syndrome in Hodgkin lymphoma is?
Minimal change
A 40 yr old man came with nephrotic range proteinuria, hematuria, dense deposits within the glomerular BM on electro microscope, immunofluorescence shows C3, no Igs
Dx? Mechanism?
Nephrotic syndrome secondary to membranoproliferative GN type 2, AKA, dense deposit disease IgG ab(termed C3 nephritic factor) directed against C3 convertase —> persistent complement activation n kidney damage
The most common extrarenal manifestation of ADPKD is?
Hepatic cyst