Week 1 Flashcards by Gillian Collom

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

How well did you know this?

Not at all

Perfectly

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
  *

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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
- TURP (transurethral resection of the prostate) if unresponsive to meds
- 5-alpha reductase inhibitors

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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
≥ 20%: “high risk”:
- initiate statin to reduce LDL-C ≥ 50%

How well did you know this?

Not at all

Perfectly

At what LDL-C level do you initiate high intensity statin with no risk assessment?

LDL-C ≥ 190 mg/dL

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Best Meds to Lower Triglycerides

Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
Niacin

How well did you know this?

Not at all

Perfectly

Best Meds to Increase HDL

Niacin
Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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
Tx:
- tx the underlying condition and aim for BP <130/80

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

Beck’s Triad

Associated with Cardiac Tamponade

elevated JVP
muffled heart sounds
systemic hypotension

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Dressler’s Syndrome

Post-MI pericarditis

tx = aspirin or colchicine

How well did you know this?

Not at all

Perfectly

Triad of R Ventricular Infarction

JVD
Clear Lungs
Positive Kussmaul Sign
1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)

How well did you know this?

Not at all

Perfectly

3 populations with atypical sxs for acute MI

elderly, women, diabetics

How well did you know this?

Not at all

Perfectly

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

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
Tx:
- cyclophosphamide + corticosteroids + plasmapheresis
  - due to high fatality → START RX while waiting for dx

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 pCO_{2 = higher than expected → additional respiratory acidosis}
if PCO_{2 = 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

Brainscape's Knowledge GenomeTM

Week 1 Flashcards

Brainscape's Knowledge Genome^TM