Renal Flashcards

Question

Overactive bladder

Answer 1

involuntary, inappropriate or excessive detrusor muscle contractions during bladder filling detrusor muscle and sphincter coordinated but muscle may be too weak to empty bladder completely

Answer 2

i.e. urethral stricture, prostate enlargement, pelvic organ prolapse, tumour compression LOW BLADDER WALL COMPLIANCE symptoms: frequency, urgery, hesitancy, nocturia

Answer 3

Benign renal adenoma Renal cell carcinoma (most common, seen in men 50-60yrs) Renal transitional cell carcinoma (rare)

Answer 4

TYPICALLY ASYMPTOMATIC (10% of cases symptomatic- weight loss, flank mass, flank pain, hematuria - suggest more severe course)

Answer 5

Cigarette smoking, obesity, uncontrolled HTN

Answer 6

Better prognosis if tumor is encapsulated Metastasis common at time of diagnosis

Answer 7

Transitional cell carcinoma (aka urothelial carcinoma) More aggressive cancer invades bladder muscle

Answer 8

-episodes of gross, painless hematuria -lower UTI symptoms (urgency, frequency, nocturia) -flank pain NOTE: MUST ALWAYS r/o malignancy with hematuria

Answer 9

-cigarette smoking -aniline dye exposure (fabric, leather, wood) -arsenic in drinking water -phenacetin ingestion (old analgesic) -uroepithelial schistosomiasis infection (parasite)

Answer 10

1) injury (immune or non-immune mediated) 2) complement deposits into glomerulus 3) immune cells recruited 4) release ROS and products which damage nephrons at all 3 levels 5) increased permeability, less filtration surface area, decreased GFR, increased Cr 6) mesangial cells swell (less blood flow) and ECF expands into Bowman space (more oncotic pressure outside glomerulus) further decreasing GFR 7) proteins and RBC can move into urine through larger pores

Answer 11

Mild: fluid expansion, edema, HTN Severe: oliguria, HTN, proteinuria exceeding 3-5g/day, nephritic sediment (RBCs, casts, leukocytes), nephrotic sediment (protein, lipids)

Answer 12

HEMATURIA with RBC casts and mild proteiuria caused by immune injury Patho: damage to capillary endothelium d/t immune deposits or autoimmune targeting of cells allowing RBCs to escape in urine

Answer 13

oliguria, less specific proteinuria, urine appears red to brown ("tea colored"), symptoms similar to nephrotic syndrome but more severe Tx: immunosuppressive therapy (i.e. high dose corticosteroid, cyclophosphorine)

Answer 14

-Acute post-infectious glomerulonehpritis (Type III hypersensitivity) -Crescentic glomerulonephritis (autoimmune rxn against basement membrane) -Lupus

Answer 15

Excretion of 3.5g or more protein in the urine per day Patho: changes to glomerular capillary or epithelium (podocytes) (thickening, sclerosis, thinning) leads to more permeability and loss of negative charge which allows proteins to enter the urine (esp. albumin and immunoglobulins)

Answer 16

-PROTEINURIA (+++) [frothy, foamy urine] -edema (less oncotic pressure in blood) -hypoalbuminemia -sodium retention (low or normal serum sodium) -dyslipidemia and lipiduria -higher infection risk -vitamin D deficiency -hypothyroidism -hypercoaguability -HTN and uremia if advanced

Answer 17

24h urine collection, low serum albumin Tx: diuretics, ACE inhibitors or ARBs for proteinuria, prophylactic anticoagulation, dietary management (moderate protein restriction, low fat, restricted salt)

Answer 18

AKI is kidney dysfunction <3 months, CKD is kidney dysfunction >3 months

Answer 19

-Increase in serum Cr >26.5 micromol in 48h -Increase in serum Cr 1.5x baseline presumed to have occured in last 7 days -Urine volume <0.5ml/kg/hr for 6h

Answer 20

Nephrons damaged by hypovolemia, decreased renal blood flow, toxins, sepsis. Local dendritic cells sense damage, release cytokines, recruit inflammatory cells and phagocytose apoptotic cells, releasing lipid mediators of inflammation.

Answer 21

Most common cause of AKI due to indirect damage from hypoperfusion of nephrons. Causes release of ADH/RAAS to retain sodium leading to oliguria. Ex: sepsis, shock, burns, hemorrhage, MI, severe N/V, renal vasoconstriction

Answer 22

Renal tubules experience direct damage from toxins that trigger inflammation. Apoptosis of nephrons forms casts that block tubules, and cause backleak leading to oliguria. Ex: less waste removal post-ichemia, nephrotoxic drugs/contrast, wastes from acute glomerulonephritis, unbound Hb in hemolytic anemia, rhabdomyolysis

Answer 23

Occurs due to bilateral obstruction of urine flow, which damages glomeruli leading to immune cell recruitment and vasoconstriction leading to oliguria. Ex: kidney stones, BPH, prostate CA, bladder outlet obstruction

Answer 24

1) vasoconstriction (RAAS activation) 2) intratubular obstruction (with necrotic/apoptotic cells) 3) tubular backleak (less permeability and vessel constriction increase pressure preventing urine from flowing out)

Answer 25

Initiation Phase: evolving injury, prevention possible Maintenance Phase: renal insufficiency, oliguria, decreased GFR and high Cr/BUN, fluid retention, electrolyte imbalances, bone disorders, hematologic symptoms, neurologic symptoms (if nitrogenous wastes buildup) Recovery phase: injury repaired, diuresis common where kidney cannot concentrate urine properly, rising GFR with lowering Cr/BUN, F/E imbalances

Answer 26

-Determine underlying cause and mitigate -Closely monitor and correct labs (I/O, electrolytes, acidosis) -Manage BP -Maintain nutrition -Prevent infection -Nephrotoxic drug stewardship -Renal replacement therapy for severe cases

Answer 27

Use: rapid mobilization of fluid in pulmonary edema, edema from renal, liver, cardiac causes. Mechanism: blocks reabsorption of Na and Cl in ascending loop of Henle. AE: dehydration, electrolyte imbalances (low K, Na, Cl), hypotension, ototoxicity Interactions: digoxin (hypokalemia), lithium, gentamicin (ototoxic), NSAIDs, antihypertensives Monitoring: F/E, weight, BP, dizziness, tinnitus/hearing loss Special populations: children okay in low doses, pregnancy risks/benefits (may reduce breastmilk), geriatrics ok (watch for AE)

Answer 28

Uses: HTN, mild-mod CHF, renal, hepatic disease; off label = renal calculi and DI Mechanism: blocks reabsorption of Na and Cl in early distal convoluted tubule Contraindications: caution with sulfa allergy, ineffective when eGFR <15-20 AE: similar to loop diuretics but less (dehydration, electrolyte imbalance), increase serum glucose and uric acid, NO OTOTOXICITY, increased risk of basal/squamous cell carcinoma Interactions: digoxin, lithium, NSAIDs Monitoring: F/E, BP, weight, skin lesions Special populations: not first line in children, safety not established in pregnancy, low dose in older adults

Answer 29

Use: conserve K+ from other diuretic use, mild diuresis Mechanism: blocks aldosterone which upregulates sodium/potassium exchange pumps. Blocking aldosterone causes K+ retention and Na+ loss. Contraindications: hyperkalemia, GFR <30ml/min, pregnancy, Addison's disease, breastfeeding AE: endocrine changes Interactions: K+ supplements/rich foods, drugs that block RAAS (ACEIs, ARBs) Special populations: AVOID children and pregnancy/breastfeeding, adjust in geri

Answer 30

Spironolactone blocks the action of aldosterone to prevent synthesis of new protein transporters for sodium and potassium (onset takes days!). Amiloride directly blocks Na/K pumps in tubules to produce more quick onset of action.

Answer 31

Modifiable: T2DM, active kidney disease, obesity, HTN, diet (high in salt and protein), pregnancy, nephrotoxin exposure Non-modifiable: age, sex (M>loss of GFR with age), congenital abnormalities, genetic factors, previous kidney injuries

Answer 32

Normally, kidney able to autoregulate and maintain stable BP in glomeruli. Prolonged damage causes loss of nephrons, capillary hypertrophy, and increase in angiotensin II. Higher pressure in glomeruli increases protein excretion, leading to more tubular protein having to be reabsorbed and which can cause fibrosis and scarring. Scarred nephrons become non-functional leading to more pressure in glomeruli.

Answer 33

Normal: kidney autoregulates (afferent arteriole constricts with high BP and dilates with low BP)- ensures consistent blood flow Capillary hypertrophy: compensates for damage of some glomeruli, experience higher pressure which causes angiotensin II release Capillary loss: continued ischemia damages all 3 layers of nephron leading to autoregulation failure Fibrosis: reduction in number of capillaries, less oxygen, more fibrosis leading to non-functional tissue

Answer 34

I: GFR >90, possible mild HTN II: GFR 60-89, HTN with slight Cr/BUN increase III: GFR 30-59, symptoms same as stage II IV: GFR 15-29, very symptomatic, HTN, anemia, electrolyte disturbances, edema V: GFR <15

Answer 35

1 or more markers of kidney damage (albuminura >3mg/mmol, urine sediment abnormalities, hematuria, electrolyte abnormalities, histologic changes, structural abnormalities on imaging, Hx kidney transplant) AND GFR <60ml/min/1.73m2

Answer 36

-Proteinuria -Increased Cr/BUN -F/E imblanaces (initial low then high Na/K with CKD progression) -Bone abnormalities (less Ca, high PO4, less active vit D) -Changes in protein, carb, fat metabolism -Anemia and hypercoaguability -HTN, dyslipidemia -Immune suppression -Headache, drowsiness, seizures -GI: ulcers, N/V, constipation, diarrhea -Endocrine: reduction in thyroid, estrogen, testosterone

Answer 37

-Healthy diet (low in processed and animal based food) -Physical activity -Weight management -Smoking cessation -Manage concurrent conditions -Pharmacotherapy (RAAS inhibitors, calcium channel blockers, diuretics, glucose management) -Renal replacement therapy, possible kidney transplant

Answer 38

kidneys fuse together into single U shape, can be asymptomatic or lead to hydronephrosis, renal calculi, or malignancy

Answer 39

Hypospadias = urethral opening on ventral side of penis, may be accompanied by chordee (penile torsion/bending) as skin becomes tethered to subcutaneous tissue and shortens Epispadias = urethral opening on dorsal side of penis

Answer 40

rare congenital abnormality causing bladder to herniate through abdominal wall diagnosed on fetal U/S, needs repair within 72h, risk for malignancy if not repaired

Answer 41

bladder opening is blocked by membrane, valve, or polyp, more common in AMAB

Answer 42

2 types: primary and secondary Primary: blockage where ureter meets renal pelvis Secondary: VUR more distally causes kinking/scarring leading to obstruction

Answer 43

hypoplasia = one or both kidneys is small with less nephrons (increased risk for pediatric CKD) dysplasia = abnormal differentiation of renal tissue from birth or due to damage post-birth

Answer 44

-Can be unilateral or bilateral, hereditary or random -Solitary kidney (one kidney), often in men, often missing L kidney, remaining kidney may be normal or abnormal leading to less functioning nephrons -bilateral renal agenesis (no kidneys) is incompatible with life, more common in men, a/w Potter syndrome, detected in utero from oligohydramnios (less amniotic fluid leads to poor lung development)

Answer 45

-Most common -Occurs post throat/skin infection with group A beta hemolytic strep -Antigen-antibody complexes + complement deposit into glomerulus and cause decrease in GFR -Manifestations: SUDDEN NEPHRITIC SYNDROME, proteinuria, oliguria, edeema, headache, vomiting, enlarged tender liver -Usually resolves with favourable prognosis

Answer 46

-Autoimmune rxn where IgA is deposited into kidney -Risk factors: family Hx of IgA nephropathy, IgA vasculitis, East Asian/white ethnicity, AMAB -Manifestations: gross hematuria with respiratory tract infection, microscopic hematuria between attacks, edema, HTN, if vasculitis also present = joint pain, abdominal pain, palpable purpura -Supportive tx, most resolve without developing CKD

Answer 47

-Primary/idiopathic (no known cause) or secondary (due to systemic disease) -Severe proteinuria, hypoalbuminemia, dyslipidemia, morning periorbital edema that shifts to dependent edema, GI symptoms (from intestinal edema- malabsorption, anorexia, diarrhea) -Associated conditions: minimal change disease (fusion of podocytes) and focal segmental glomerulosclerosis (damage to glomerular capillaries)

Answer 48

-Most common cause of AKI, especially children <4 -Characterized by hemolytic anemia, thrombocytopenia, AKI -Linked to bacterial (E. coli) toxins and viruses -Toxins damage glomerular arterioles leading to inflammation and fibrin clots -Clots narrow vessels and break down RBCs, also use up platelets (thrombocytopenia) -Broken RBCs taken up by spleen (anemia) -Blood flow to kidneys interrupted leading to AKI -Manifestations: GI ILLNESS (fever, vomiting, diarrhea), pallor, purpura, DIARRHEA (BLOODY/WATERY), oliguria, JAUNDICE, CNS symptoms (azotemia)

Answer 49

-Most common pediatric renal tumor -Arises from undifferentiated mesoderm (may be present with other abnormalities such as lack of iris, horseshoe kidney) -Sporadic (most common) or inherited (rare) -Main symptom is non-tender, palpable mass on one side of abdomen (can also have vague abdo pain, anemia, hematuria, fever) -More common in Black children than White children

Answer 50

-Short ureter is not compressed by muscle/submucosa when bladder contracts leads to urine backflow into ureter increasing risk for infection. -More common in females -Suspect if recurrent UTIs, unexplained fever, poor growth/development -Can cause LT issues if not corrected (i.e. scarring, HTN, CKD)

Answer 51

Intermittent passage of urine at inappropriate time or place in children >5 Classified as: diurnal enuresis (daytime) or nocturnal enuresis primary (never achieved full bladder control) or secondary (achieved control for 6 months before developing incontinence)

Answer 52

4-7 voids/day UTIs, congenital defects, diabetes, CKD, constipation, psychologic stress, GI conditions, ADHD, sleep conditions, genetic factors

Answer 53

PO/IV: unchanged (unless diabetic gastroparesis, antacids, edema) SC: may be reduced with edema NO OR MINIMAL CHANGE

Answer 54

Less protein and more total body water affect distribution; if patient is dehydrated it has opposite effect Hydrophilic drugs- lost in excess fluid Hydrophobic drugs- cannot get past edema to target site KEEP DOSE SAME OR SLIGHTLY HIGHER- FIRST DOSE ONLY

Answer 55

Often need to be higher or normal dose to account for changes in distribution

Answer 56

Less proteins = more free drug able to exert effect DECREASE DOSE

Answer 57

DECREASE DOSE Less metabolism by kidneys and liver (damaged by or occupied with uremic wastes leading to less activity)

Answer 58

Drug elimination is impaired if kidneys are damaged DECREASE DOSE

Answer 59

Keep dose same, extend dosing interval e.g. aminoglycosides, fluoroquinolones

Answer 60

Lower dose, keep interval same e.g. penicillins, oxazolidinones, cephalosporins, carbapenems, macrolides, vancomycin

Answer 61

Wide TI: may not need to change dose if prophylactic, adjust if excess associated with toxicity Narrow TI: need close monitoring, adjust every dose except first

Answer 62

Sex: body composition/sex hormones can influence pharmacokinetics, AFAB less likely to be diagnosed with CKD Age: avoid nephrotoxic drugs in peds/geri populations; adjust doses Pregnancy: may lead to alt drug distribution and mask early renal dysfunction Illness: can cause changes to drug pharmacokinetics/dynamics, onc patients may have sarcopenia and alt distribution (higher Cr), dialysis will promote clearance of some drugs

Answer 63

Apixaban 1st line for CKD V, other direct acting oral anticoagulants OK in CKD III/IV with adjustment Unfractionated heparin best injectable

Answer 64

SGLT-2 inhibitors show kidney benefits but less effective when eGFR <30 GLP agonists do not need dose adjustment Current recommendations: eGFR >30: metformin + SGLT2 eGFR <30: GLP-1, DDP4, do not necessarily need to stop SGLT-2 Basal insulin best

Answer 65

ACE inhibitors/ARBs: preferred in proteinuria, risk of hyperkalemia Calcium channel blockers: okay for hypertension Thiazide diuretics: 1st line without albuminuria, may need to switch to loop diuretic in later stage CKD Beta blockers: renally excreted, ok for stable CKD MRAs: used in patients with low serum potassium

Answer 66

No dose adjustment: acetaminophen (preferred), TCAs (anticholinergic SE) Need adjustment: gabapentin, duloxetine, venlafaxine Worst: PO NSAIDs contraindicated in CKD V, need close monitoring in earlier stages, topicals ok

Answer 67

Preferred: hydromorphone, fentanyl, methadone, transdermal buprenorphine Not preferred: oxycodone, morphine, codeine, tramadol

Renal Flashcards

(91 cards)