Week 1 Flashcards
Stress Incontinence Tx
- kegel exercises: 3-6 weeks of daily exercises, 200/day
- vaginal estrogens
-
pessary
- SEs: vaginal irritation, foul-smelling discharge, UTIs
- surgery → mid-urethral sling
- weight loss
Prostate Cancer Etiology, S/sxs, PE, Dx, Tx
- most are adenocarcinomas
- associated with the BRCA1 gene
- Risk factors: african american, old age, family hx
-
S/sxs: urinary retention (more likely sign of BPH), decrease in urine stream strength
- back pain (metastatic disease)
- painful ejaculation
- PE: DRE: hard, nodular, enlarged, and asymmetrical prostate
-
Dx:
- indications for transrectal biopsy with normal rectal exam → PSA > 10 or abnormal transrectal U/S
- PSA > 4: U/s with needle biopsy
- PSA >10: bone scan to r/o metastases
-
Tx;
- radical prostatectomy → complication = erectile dysfunction & urinary incontinence
- with metastases: need androgen deprivation therapy (leuprolide) → type of medical castration, but can be reversible
*
Calcium Nephrolithiasis Risk factors and Prevention
- calcium oxalate = most common
- Radiopaque
- Risk factors: decreased fluid intake, high urinary calcium or pH, high animal protein intake, hypercalcemia, males, medications (loop diuretics, acetazolamide, antacids)
- Prevention: increased fluid intake, thiazide diuretics, citrate, low sodium diet, decreased animal protein diet
When to screen for PSA
DISCUSS WITH PATIENT
- men age 55-69 yo
- 50 years old if first degree family hx
- 45-50 if african american
BPH S/sxs, PE, Dx, & Tx
Benign Prostatic Hyperplasia
- 50% of men have BPH by age 60, >90% by age 85
-
S/sxs: difficulty starting stream, post-void dribbling, hesitancy (start and stop)
- nocturia
- weak urinary stream
- PE: digital rectal exam → uniformly enlarged firm and rubber prostate
-
Dx:
- DRE +PSA
- PSA < 4 = normal
- PSA > 4 → BPH, prostate cancer, prostatitis
- UA to r/o other causes
-
Tx:
- if mild → watchful waiting
-
alpha blockers can provide the most rapid relief (smooth muscle relaxation of porstate and bladder neck
-
tamsulosin, prazosin, terazosin (shrink size of prostate)
- finasteride & dutasteride
-
tamsulosin, prazosin, terazosin (shrink size of prostate)
- TURP (transurethral resection of the prostate) if unresponsive to meds
- 5-alpha reductase inhibitors
UTI prevention
- drink adequate amount of water
- avoid delay in voiding
- personal hygiene
- cranberry juice/tablets
- abx prophylaxis for 3 UTIs/12 months
- Bactrim/Cipro
Major Risk Factors of Coronary Artery Disease (CAD)
- Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
- Smoking (Most important modifiable risk factor)
- Hyperlipidemia, HTN
- Men >45yo, Women >55yo
- Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)
Post MI Complications
- Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
- VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
- Acute Mitral Regurg: shock, apical murmur, pulmonary edema
- new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins
Acute vs. Chronic Heart Failure
-
S/sxs:
-
Chronic Heart Failure (compensated):
- congestion
- laterally displaced apical impulse
-
Acute Heart Failure:
- breathlessness
- rapid weight gain
- fluid build-up in the lungs and around the body
- inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal
-
Chronic Heart Failure (compensated):
Systolic Heart Failure
-
Definition: heart failure with decreased ejection fraction
- impaired contractility
- thin ventricular walls (DILATED)
- S3 gallop (sys-tol-ic)
-
Etiology:
- ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis
Diastolic Heart Failure
-
Definition: Heart failure with preserved ejection fraction
- impaired filling/relaxation
- thick ventricular walls (**Hypertrophied**)
- S4 gallop (Di-a-stol-ic)
-
Etiology:
- HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring
Tx of Heart Failure
- **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
-
Long Term Tx (Afterload reduction:
- ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
- Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
- Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
- Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
-
Long Term Tx (Preload Reduction)
- Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
- potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
- Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
-
Long Term Tx (Positive Inotropes):
- Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF
Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus
10-year ASCVD risk percent begins risk discussion:
-
<5%: “low risk”
- emphasize lifestyle to reduce risk factors
-
5-<7.5%: “borderline risk”:
- If risk enhancers present then risk discussion regarding moderate-intensity statin therapy
-
≥7.5-<20%: “Intermediate Risk”
- Risk discussion:
- if risk estimate + risk enhancers favor statin, initiate moderate-intensity statin to reduce LDL-C by 30-49%
- if unsure, can use CAC score
- Risk discussion:
-
≥ 20%: “high risk”:
- initiate statin to reduce LDL-C ≥ 50%
At what LDL-C level do you initiate high intensity statin with no risk assessment?
LDL-C ≥ 190 mg/dL
Best meds to lower elevated LDL
-
Statins (Rosuvastatin, atorvastatin, etc) → inhibit HMG Co-A reductase
- impair production of cholesterol in the liver → upregulation of LDL receptors
-
Bile Acid Sequestrants (Cholestyramine, colesevelam, colestipol) & Cholesterol absorption inhibitors (Ezetimibe)
- impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors
Best Meds to Lower Triglycerides
- Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
- Niacin
Best Meds to Increase HDL
- Niacin
- Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
Abnormal Lipid Values
- Low HDL <40 mg/dL
- High LDL > 190 mg/dL
- high LDL in diabetic >70 mg/dL
- high total cholesterol >250 mg/dL
- high fasting triglyceride >150 mg/dL
Secondary HTN Definition and Causes
- Definition: SBP ≥130 and/or DBP ≥80 WITH identifiable cause
-
Causes:
- Primary aldosteronism = MOST COMMON
- renal vascular disease
- pheochromocytoma
- adrenal tumor that secretes catecholamines (ie norepi and epi)
- Cushing’s Syndrome
- activation of the renin-angiotensin system
- Congenital Adrenal Hyperplasia
- Hyperthyroidism
- Myxedema
- associated with hypothyroidism
- Coarctation of the Aorta
- Excessive alcohol intake
- Use of Oral Contraceptives
Secondary HTN Red Flags, Dx, & Tx
-
Red Flags:
- HTN at an early age <25 without a family hx
- HTN first develops >50 yo
- previously controlled now refractor
- Pt is refractory on antihypertensive medications or has severe BP
-
Dx:
- when HTN is newly diagnosed consider ordering:
- urinalysis
- spot urine albumin: creatinine ratio → albuminuria ratio = >30mg/day
- indicative of CKD
-
Blood tests
- creatinine, K, Na, fasting glucose = BMP
- lipid panel
- TSH
- EKG
- when HTN is newly diagnosed consider ordering:
-
Tx:
- tx the underlying condition and aim for BP <130/80
Acute Bacterial Endocarditis Definition and organism
- Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
- Rapidly destructive (fatal < 6 weeks if untreated)
Beck’s Triad
Associated with Cardiac Tamponade
- elevated JVP
- muffled heart sounds
- systemic hypotension
Mnemonic to Remember Medical Tx of STEMI
MOAN & BASH
Morphine, oxygen if O2 <90%, Aspirin 162 mg, Nitro q 5 min (don’t give to pts with systolic <90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload)
Beta blockers (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; Contraindication in Heart block, high risk for cardiogenic shock) , ACE-I/ARB (more for long term use → improve L ventricular EF, mortality rate), Statin, Heparin (antithrombotic therapy → impede progression of thrombus in coronary artery)
TPA if pt cannot have reperfusion from cath lab in <90minutes from door to lab
Dressler’s Syndrome
Post-MI pericarditis
tx = aspirin or colchicine
Triad of R Ventricular Infarction
- JVD
- Clear Lungs
-
Positive Kussmaul Sign
- paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)
3 populations with atypical sxs for acute MI
elderly, women, diabetics
Heliotrope Sign (associated with Dermatomyositis**)
-
dermatomyositis = autoimmune disease that leads to degeneration of the skin and muscle
- characterized by muscle weakness heliotrope sign and Gottron’s Papules
Gottron’s Papules (indicative of Dermatomyositis**)
- dermatomyositis = autoimmune disorder that leads to the degeneration of the skin and muscle
- characterized by muscle weakness and Gottron’s papules and Heliotrope sign
- Gottron’s papules = over the joints of the hands
Butterfly/Malar Rash
- indicative of Systemic Lupus Erythematosus
- worsened when exposed to the sunlight
- systemic lupus erythematosus also will show a rash on the hands that spares the knuckles
Net Effect of Increased PTH
hypercalcemia, hypophosphatemia
Causes of Pre-Renal Acute Renal Failure
- due to volume loss, heart failure, or loss of peripheral vascular resistance → all lead to loss of perfusion in kidneys
- NSAIDs also can cause this (vasoconstriction of the afferent arteriole)
- ACEI and ARB block effect of angiotensin (vasodilation of the efferent arteriole)
- Diuretics
- ***Kidneys are working fine, the organs that perfuse the kidneys arent working properly***
PreRenal Acute Renal Failure S/sxs, Dx, and Tx
- S/sx: weak oliguria (decreased urine output), dizziness, sunken eyes, tachycardia, orthostatic BP changes
- Dx: BUN:Cr > 20:1, urine osmolality > 500, FeNa <1%, FeUrea <35%, Urine Na <20 mEq/L
- Tx: tx with fluids, cardiac support, and/or tx shock
PostRenal AKI Etiology, S/sxs, dx, tx
- Etiology: obstruction (most common = prostate), bilateral outlet obstruction or bilateral ureteral obstruction
- S/sxs: oliguria or anuria +/- suprapubic pain
-
Dx: foley catheter placement to find source of obstruction
- if large urine output after foley = bladder, urethra, BPH
- if low urine output after foley = ureter obstruction or pathology
- Renal U/S but CT is most specific!!
- tx: removal of obstruction → if done rapidly = quick reversal of AKI
Acute Tubular Necrosis Etiology
- ***Type of Intrinsic AKI***
- Etiology = kidney ischemia or toxins
- prolonged pre-renal AKI = most common cause
-
Major Causes:
- drugs and toxins: ampho B, cisplatin, sulfa drug, aminoglycosides, radiocontrast media, NSAIDs, ACEI, cocaine use
- ischemic related ATN : dehydration, shock, sepsis, hypotension
- endogenous toxins: heme from hemolysis, myoglobin from rhabdomyolysis (iron is myoglobin is toxic to renal epithelial cells), tumor lysis syndrome, muscle breakdown in a marathon runner
Acute Tubular Necrosis S/sxs, Dx, Tx
- S/sxs: Oliguria, increased SCr etc
-
Dx: urinalysis = muddy brown casts (renal tubule epithelial cells), myoglobinuria, hemoglobinuria
- FeNa >2%, FeUrea >35%, Urine Osmolality <350
-
Tx: remove toxin or re-perfuse kidney via IV fluids
- can use loop diuretics if pt is euvolemic and not urinating
- ***most pts return to baseline within 7-21 days ***
Etiology of Interstitial Nephritis
- Etiology: immune-related response
- due to:
- drugs: PCN, sulfa (bactrim), NSAIDs, phenytoin, Diuretics, etc
- immunologic & infx disease: strep (get an ASO antibody), SLE, CMV, Sjogren’s, sarcoidosis
Interstitial Nephritis S/sxs, Dx, & Tx
- ***type of intrinsic AKI***
- S/sxs: oliguria, increased SCr
-
Dx: urinalysis = WBC cats, WBCs, and eosinophils
- acute azotemia (accumulation of nitrogenous waste, BUN)
- diagnosed with RENAL BIOPSY → interstitial inflammatory cell infiltrates
-
Tx: d/c offending drug, corticosteroids, dialysis PRN
- → usually self-limiting if caught early
- most people recover kidney function within 1 year
Etiology of Nephrotic Syndrome
- glomerular damage results in higher loss of proteins in the urine
-
Most common primary causes:
- membranous nephropathy: most common in non-DM adults associated with malignancy
- MINIMAL CHANGE DISEASE: most common cause in children, idiopathic nephrotic syndrome sxs improve after tx
- focal segmental glomerulosclerosis: obese pts, heroin, and HIV (+) black males
-
Most common Secondary Cause:
- lupus
- DM
Nephrotic Syndrome S/sxs, Dx, & Tx
- S/sxs: peripheral or periorbital edema, ascites, weight gain, fatigue, and HTN, frothy urine
-
Dx: serologic testing and renal biopsy
- proteinuria >3.5g/day = diagnostic ( 24h urine collection)
- urinalysis: free lipid or oval fat bodies or fatty casts → lipiduria
- Hypoalbuminemia < 3.5g/dL
- hyperlipidemia LDL > 130mg/dL, Triglycerides > 150mg.dL
-
Tx:
- tx the causative disorder, corticosteroids
Etiology of Glomerulonephritis
- inflammation of the glomeruli due to blockage from immune complexes → immune response causes this
- Post-Infectious Group A strep → diagnosed with ASO titers and low serum complement
-
IgA Nephropathy (berger disease): Most common cause of acute glomerulonephritis
- young males after URI or GI infx (within 24-48 hours) → IgA immune complexes are first line defense in respiratory/GI secretions so infx → overproduction which damages the kidneys
- more common in asian population
-
Membranoproliferative Glomerulonephritis: caused by SLE, viral hepatitis (Hep C)
- secondary to immune-complex deposition or complement mediated mechanism
Glomerulonephritis S/sxs, Dx, & Tx
- S/sxs: edema + HTN + hematuria + RBC casts, jaundice, HTN
-
Dx: urinalysis = hematuria >3 RBCs/HPF + RBC casts + proteinuria (1-3.5g/day)
- ASO titer for post-strep
- serum complement = decreased (not always
- RENAL BIOPSY = GOLD STANDARD
-
Tx: steroids and immunosuppressive drugs to control inflammation due to immune response
- dietary management = salt and fluid restrictions
- Dialysis if symptomatic azotemia
- ACEI/ARBs (enalapril or losartan) are renoprotective → BP goal <130/80
- use meds to control hyperkalemia
Definition of CKD
dx: GFR < 60mL/min/1.73m2 for 3 months or any of the following:
- albuminuria: urine albumin: creatinine ratio >30mg/day
- proteinuria: urine protein: creatinine ratio > 0.2
- hematuria
- structural renal abnormalities ( solitary kidney, hx of abnormal renal histology hx of renal transplant)
Etiology of CKD
- Diabetes = MOST COMMON CAUSE (30%)
- HTN (25%)
- chronic glomerulonephritis (15%)
- interstitial nephritis, polycystic kidney disease, obstructive uropathy
S/sxs of CKD
- Pruritus = common, but difficult to tx
- Cardio: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis
- GI: (usually due to uremia) nausea, vomiting, loss of appetite
- Neuro: lethargy, confusion, tetany → (due to hypocalcemia), uremic seizures, peripheral neuropathy
-
Heme: normocytic, normochromic anemia (secondary to deficiency of erythropoietin)
- bleeding secondary to platelet dysfunction→ platelets do not degranulate in uremic environment
-
Endo/Metabolic:
- Ca2+/Phosphorus disturbances→ decreased renal secretion of phosphate leads to hyperphosphatemia → decreased production of 1,25-dihydroxy vitamin D → hypocalcemia → hyperparathyroidism
- hyperkalemia → decreased secretion and acidosis
-
Fluid & Electrolyte problems:
- volume overload: watch for pulm edema
- hyperkalemia: due to decreased urinary secretion
- hypermagnesemia: secondary to reduced urine secretion
- hyperphosphatemia: decreased clearance of phosphate
- metabolic acidosis: due to loss of renal mass (& therefore decreased ammonia production) & kidneys’ inability to secrete H+
Tx of CKD
- Tx: ACEI and ARBs → slow progression of renal dysfunction
- manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation
- Maintain HGB at 11-12 g/dl → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality
- Dietary management: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus
- Need for hemodialysis or kidney transplant
- PCV-23
- Fluid overload management: dietary salt <2 gm/day
- GFR > 30 → thiazide diuretics (hydrochlorothiazide, chlorthalidone)
- GFR <30 → loop diuretics (furosemide, torsemide, bumetanide)
- can use phosphorus binders to reduce hyperPTH → calcium carbonate, calcium acetate, sevelamer, lanthanum, iron
- tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level >22
NSAIDs and Sodium
NSAIDs reduce renal prostaglandins
and prostaglandins inhibit the action of ADH
so NSAID use can increase action of ADH and cause increased water reabsorption
Desmopressin (DDVAP)
synthetic analogue of ADH
Act on V2-receptors at the collecting duct → reabsorption of water
used to tx central diabetes insipidus → the underlying pathophys behind isovolemic hypernatremia
Hypokalemia Tx
When to tx? <3.5 mEq/L and/or pt is symptomatic
- treatment:
- oral: K-chloride, KPO4, K-acetate, K-citrate, k-gluconate
- IV: if >10 mEq/L should be monitored via telemetry
- other: diuretic induced (spironolactone- K+ sparing diuretic)
- correct hypomagnesemia
- ****low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently*****
- correct acid-base imbalance
- correct hypomagnesemia
- oral: K-chloride, KPO4, K-acetate, K-citrate, k-gluconate
Goodpasture’s Syndrome
- causes rapidly progressive Glomerulonephritis (nephritic syndrome)
- anti-glomerular basement membrane
-
presentation:
- lungs/kidneys hemorrhage
- teenagers & >50 years
- rapidly progressive→ fatal
-
Pathology:
- antibodies against the glomerular basement membranne
- often associated with crescent formation
- antibodies against the glomerular basement membranne
-
Tx:
-
cyclophosphamide + corticosteroids + plasmapheresis
- due to high fatality → START RX while waiting for dx
-
cyclophosphamide + corticosteroids + plasmapheresis
Hemolytic Uremic Syndrome
-
Presentation:
- E.coli O157:H7 (foodborne), Salmonella, etc. → undercooked meat consumption
- bloody diarrhea that has resolved
- fever; low platelets; AKI
- Dx:
- often via serum assays
-
Treatment: symptomatic manage,ent
- HUS may require dialysis, 10% death rate
Pauci-Immune Vasculitis S/sxs & Tx
- type of nephritic syndrome → cause of rapidly progressive glomerulonephritis
- Presentation: hematuria + signs of necrotizing small vessel vasculitis (diffuse skin lesion, lung hemorrhage, sinusitis, etc.)
- Tx: aggressive tx with steroids, cyclophosphamide or rituximab
- plasmapheresis → severe disease
Lupus Nephritis S/sxs & Tx
-
S/sxs: usually hx of lupus
- SLE more common in female AA population
- proteinuria, hematuria, + elevated creatinine
- Tx: dependent on biopsy classifications
Dipstick positive for hemoglobin and myoglobin but no RBCs?
Rhabdomyolysis
Normal Urine protein/creatinine ratio
< 0.2 or 200
aka SPOT urine protein/SPOT urine creatinine
Normal Urine 24 hour protein
<200mg/day
Microalbuminuria
30-300mg/g
Macroalbuminuria
>300mg/g
Rapidly Progressive Glomerulonephritis (RPGN)
when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks
-
Nephritis:
- RBC casts
- proteinuria <3.5g
Non-Oliguria vs Oliguria vs Anuria
Non-oliguria: >400mL/day
Oliguria: 100-400 mL/day
Anuria: <50mL/day
Indications for Acute Dialysis
A: severe metabolic Acidosis
E: Electrolyte Problems (Hyperkalemia)
I: Intoxication (Antifreeze)
O: Overload of fluids
U:Uremic symptoms (pericarditis, altered mental status)
At what GFR should we refer to nephrology?
GFR <30 ml/min/1.73m2 *CKD stage 4-5)
Winter’s Formula
to calculate expected pCO2
- Expected pCO2 = (1.5 x bicarb) + 8 +/- 2
- if pCO2 = higher than expected → additional respiratory acidosis
- if PCO2 = lower than expected → additional respiratory alkalosis
Albuminuria
urine albumin: creatinine ratio >30 mg/g (per day)
Aldosterone
Causes K excretion in principal cells of renal Collecting Duct and K reabsorption in intercalated cells of CD
ACEI/ARBs in CKD
1st line therapy for HTN in early CKD as they “tell kidneys to take a break & not filter so hard”
Will cause slight incr in SCr. Expected and ok as long as <30% and proteinuria is improving.
Watch K as ACEi/ARB can increase
Do not use ACEi & ARB together d/t incr risk of AKI, hyperkalemia, hypotension
