Renal Pathophysiology Flashcards
1) Causes of Chronic Kidney Disease
2) What is used to diagnosed Chronic Kidney Disease?
3) When do symptoms occur in Chronic Kidney Disease?
4) Clinical manifestations
1) Diabetes, Hypertension, Glomerulonephritis, Lupus -> Permanent loss of nephrons
2) GFR is estimated using serum creatinine. Excretion of albumin in urine is used as marker (Dipstick)
3) Very late, not until disease is far advansed (We have 2 kidneys, and kidneys have great compensatory ability)
4) Accumulation of nitrogenous waste (Azotemia, Urea in blood) Fluid, electrolyte and acid/base disorders (Unregulated Na+ secretion, Increased K+ in blood) Secondary Hyperparathyroidism. Skeletal disorders. Anemia. Coagulopathies. Cardiovascular (Hypertension, Heart disease, Pericarditis). GI symptoms (Uremia -> Anorexia, nausea, vomiting). Neuromuscular (Peripheral neuropathy). Decreased immune system. Sexual dysfunction. Impaired drug elimination.
1) What is renal calculi and what is it the most common cause of?
2) What things are required for stone formation?
3) What different kinds of stones are there and which is the most common?
4) Most common symptom of renal calculi and when the symptoms appear
1) Stones: Aggregates of material that the kidney normally excreads. It is the most common cause of upper urinary obstruction
2) Supersaturated urine + environment that allows growth. A nidus/nucleus to form stone around
3) Calcium stones, Uric stones, Magnesium ammonium phosphate stones (Struvite stones), Cystine stones
4) Pain. When stones becomes lodged in ureter and causes obstruction OR When stone causes distension of the renal pelvis
1) Who are most affected by UTIs and what are the risk factors?
2) What defences do we have against UTIs? Including defencens of women, men and bladder in general
3) Clinical manifestations of lower uncomplicated UTI
1) Young women Risk factors Prior UTI, New sex partner, vaginal pH changes, urinary obstruction, impaired bladder emptying, catheterization, diabetes
2) Men Length of urethra, antibodies in prostatic fluid Women Periurethral area flora Bladder Washout phenomenon, Bladder lining as barrier, immune response (IgA+phagocytes)
3) Frequent urination, lower abdominal/ back discomfort, burning with urination, sometimes fever
1) What is urinary incontinence? And who are most often affected?
2) Describe stress incontinence including what causes it in women and men
3) Describe overactive bladder/urge incontinence including the 2 mechanisms behind
4) Who are most in risk of bladder cancer and what can cause it?
1) Involuntary loss/leakage of urine. Older people, most often men
2) Loss of urine when intra-abdominal pressure increases (coughing, laughing, sneezing) Women PUV angle is important. Aging -> Loss of angle -> incontinence. Childbirth, surgery Men Prostate disease, surgical, neurological
3) Loss of urine due to strong desire to void (Involuntary contraction during filling). Frequent urinarions, dysuria, nocturia. 2 mechanisms Neurogenic (Parkinsons, MS, stroke): Damage to inhibitory nerve pathway -> triggers blader. Myogenic (Smooth muscle): Increased excitability of the muscle cells
4) Elderly men. Etiology Products from dye industry, smoking, chronic bladder infections, bladder stones
1) What is glomerulonephritis?
2) Etiology including most common origin
3) The 2 immune mechanisms implemented in the development
4) Cellular changes
5) Glomerular changes (What parts can be affected)
1) Inflammation of the glomerular structures in the kidneys
2) Immune origen (Both primary and secondary). Secondary causes: Diabetes, Hypertension, Toxins. Few are hereditary
3) 1. Injury from antibodies reacting with glomerular antigens. 2. Injury from circulating antigen-antibody complexes that becomes trapped in the glomerular membrane
4) Increased number of glomerular and immune cells, basement membrane thickening, sclerosis and fibrosis
5) Diffuse - All glomeruli and all parts, Focal - Some are affected, others are normal, Segmental - Only involves certain segments of glomeruli, Mesangial - Only involves mesangial cells
Describe the idea/functionality behind dialysis
Semipermeable capillaries/ peritoneal cavity is used to filter metabolic end products of the body
1) What characterizes Nephrotic syndrome?
2) Pathogenesis of Nephrotic syndrome
3) Symptoms of Nephrotic syndrome
4) Etiology of Nephrotic syndrome
1) Massive proteinuria, lipiduria, hypoalbuminemia, edema, hyperlipidemia
2) Glomerular damage -> Increased glomerular permeability -> Proteinuria. This leads to: Hypoalbuminemia -> Decreased osmotic pressure -> Edema. Loss of binding proteins -> Decreased hormone and Ion in plasma. Decreased globulins -> Increased infection risk. Increased synthesis of proteins by liver -> Hyperlipidemia
3) Pulmonary edema -> Dyspnea, Increased LDL -> atherosclerosis
4) Primary Minimal change disease, glomerulonephritis Secondary Diabetes, lupus
1) What is hydronephrosis and how does it happen?
2) Clinical manifestions
1) Obstruction of urine outflow -> Urine filled dilation of renal pelvis + progressive atrophy of kidney
2) Recurrent UTIs. Often no symptoms, pain, anuria, renal failure, polyuria, nocturia
1) What are urinary obstruction classified on? (4 things)
2) Describe the compensatory and de-compensatory stages of urinary obstruction
1) Cause (congenital/acquired), Degree (partial/complete), Duration (Acute/Chronic), Level (Upper/lower)
2) Compensatory (Early stage): Hypertrophy + Hypersensitivity of bladder, Decreased suppression of urination
Decompensatory (Later): Bladder muscle not strong enough -> residual urine in bladder. Frequent urination + weak stream
1) What is polycystic kidney disease?
2) Describe Autosomal dominant PKD including who it “hits”, pathogenesis and manifestations
3) Describe Autosomal recessive PKD including manifestations
1) Group of disorders characterized by fluid-filled sacs in the tubular structures of the kidneys
2) Adults. Fluid filled sacs in kidneys + other organs. Pathogenesis Cysts in tubules from epithelium -> Cell lining: (Proliferation + Decreased differentiation) + Defect basement membrane -> Cysts growth + Can detach from endothelium. ** Manifestations** Slow progression -> Renal failure in 40’s. Initially: Asymptomatic. Progression: Pain, hematuria, enlarged kidneys, distorted surface.
3) Cystic dilation of tubules in kidneys (Smooth surface) Affects infants. Manifestations Large kidneys -> Decreased lung development, Bilateral flank mass, Acute renal failure, Hypertension
