BMS Final PDF

Study all endocrine (30 questions) and kidney system (10 questions) Extrapelvic ○ Pituitary gland Intrapelvic ○ Kidneys Retroperitoneal organ (only organ to be known as) Weighs around 150 gm ○ Ureters (2) ○ Urinary bladder ○ Uretha Major function ○ 1. Regulation Blood volume and composition Blood pr...

Study all endocrine (30 questions) and kidney system (10 questions) Extrapelvic ○ Pituitary gland Intrapelvic ○ Kidneys Retroperitoneal organ (only organ to be known as) Weighs around 150 gm ○ Ureters (2) ○ Urinary bladder ○ Uretha Major function ○ 1. Regulation Blood volume and composition Blood pressure Blood pH ○ 2. Hormone production Erythropoietin Renin ○ 3. Elimination of metabolic waste products Anatomy ○ ○ 1. Cortex Outer cortical Inner juxtamedullary ○ 2. Medulla 3. Renal pyramids 4. Renal papilla 5. Major and minor calyx 6. Renal pelvis ○ 7. Ureter Nephron ○ Functional unit of the kidney ○ Major functions Glomerular filtration Tubular secretion Tubular reabsorption Renal Diseases Congenital anatomical abnormalities Double collecting system (1:150) Horseshoe kidney ○ Usually occurs in association of other genetic disease as 47; +18 Edward’s Syndrome ○ Duplication anomalies Supernumerary collecting systems ○ Unilateral or bilateral ○ May involve the renal pelvis and ureters (accessory renal pelvis, double or triple pelvis and ureter), calyx, or ureteral orifice ○ Duplex kidneys ○ Fused kidneys ○ Surgery Fusion anomalies Horseshoe kidney (difficult b/c cannot separate) ○ The most common ○ The kidneys are joined, but the ureters enter the bladder on each side ○ Generally drain well ○ Surgery Cystic disease of the kidney Simple cyst (acquired non-significant) Polycystic disease of the newborn (Autosomal Recessive) ○ Associated with hereditary diseases Oliguria (less quantity of urine) Notices when baby is not urinating as often Polycystic disease of the adult (Autosomal Dominant) ○ Easier to dx Common symptoms of renal disease Urinary frequency? Urgency? Systemic conditions/disease? Pain? Hesitance? Abnormal discharge? History of infections? History of STD Symptoms (KIDNEY) ○ Dysuria ○ Nocturia ○ Hematuria (macro and micro) ○ Obstruction ○ Enuresis ○ Polyurea ○ Anuria ○ Oliguria Laboratory tests U/A - urine analysis ○ SG (Specific Gravity) = b/w 1.002 and 1.035 ○ pH = 4.5 - 8 ○ Color = clear/yellow ○ Proteins, RBC, Glucose, Bacteria, Yeast, Parasites, Nitrates, urinary casts U/C - urine culture (not all patients get this) ○ Common bacteria: E. Coli ○ Frequent UTIs -> order urine culture CMP - levels of creatinine, albumin Creatinine clearance (independent test) - in HTN diseases Urinary Tract Infection (UTI) A broad term describing microbial colonization of the urine and infection of any of the components of the urinary tract ○ Urethra, bladder, ureters, renal pelvis, kidneys Divided into ○ Asymptomatic bacteriuria (AB) ○ Uncomplicated UTI ○ Complicated UTI ○ Acute pyelonephritis UTI is among the most common predisposing causes of bacteremia and sepsis Asymptomatic Bacteriuria Prevalence: women of childbearing age (6%) Most common infecting organism is E. Coli Resolve spontaneously Pregnancy screening and treatment are essential in prenatal care Untreated 40% risk for UTI and a 20% to 60% risk for acute pyelonephritis in late pregnancy, prematurity and low birth weight In diabetic women, incidence up to 18% Uncomplicated UTI (Acute Cystitis) Extremely common Young, sexually active women have about 0.5 episodes per person-year ○ E. Coli is responsible (80%) ○ Staphylococcus saprophyticus (18-20%) Enterobacteria in the vagina and periurethral zone colonize the urethra ascending into the bladder mucosa Proliferation in the urine incite an inflammatory response The shorter urethra in women may help explain why women are more susceptible than men Uropathogens (E. Coli) have special characteristics that facilitate colonization and invasion Symptoms ○ Dysuria, frequency, urgency, suprapubic discomfort (tenderness), hematuria Diagnosis ○ History, physical exam, temperature (low-grade fever), abdominal exam (costovertebral angle tenderness), urine exam Urine dipstick Leukocyte positive ○ Indicates pyuria = infection Nitrate ○ When positive, indicates the presence of enterobacteria, which convert nitrate to nitrite Urine culture Not routinely done with uncomplicated UTI (unless it fails to resolve with treatment, relapses after treatment, or frequency recurrence) Imaging studies are necessary Recurrent UTI Most commonly represent reinfection with the same agent ○ Epidemiology ○ Clinical presentation ○ Treatment Most recurrences occur within 3 months ○ Singel recurrences are common In those predisposed ○ Frequency of sexual intercourse ○ Use of the diaphragm-spermicide combination ○ Recent antibiotic use with a history of UTI Complicated UTI Occur in pregnancy Underlying diseases: Diabetes Institutionalized patients Structural or functional abnormalities of the urinary tract (obstruction, stones, indwelling urinary catheters) During pregnancy, focus is on detecting asymptomatic bacteriuria (by urine culture) preventing UTI and acute pyelonephritis in late pregnancy Predisposing factors ○ Dilation of the ureters ○ ○ Forward displacement of the bladder as the uterus enlarges Incomplete emptying More complicated in men because they do not present with typical symptoms ^ Diabetics usually have uncomplicated UTI Increased risk for ○ Severe acute cystitis ○ Acute pyelonephritis complicated ○ Patients who are also immunocompromised Predisposing factors ○ Impaired bladder emptying ○ Impaired leukocyte function ○ Focal damage to the kidney due to diabetic microangiopathy Spinal cord injuries Demyelinating disease ^ patients have no feeling and do not know they are presenting symptoms Chronic indwelling catheters should be avoided ○ Intermittent (4 times/day) in-and-out catheterization UTI in the debilitated elderly patient is usually complicated and accompanied by concomitant disease and bladder malfunction, incontinence, or indwelling catheters UTI accounts for more than 50% of episodes of bacteremia in institutionalized elderly patient, often in those with long-term indwelling catheters Etiologic organisms Resistant strains of E. Coli Enteric gram-negative organisms Pseudomonas Staphylococcus aureus Enterococci Yeast Fungi Acute pyelonephritis Suppurative inflammation of the kidney and renal pelvis usually Principal offending organisms are enteric gram (-) bacteria, E. Coli, Proteus, Enterobacter 1. Secondary to ascending bacterial infection (urinary bladder, ureter, or urethra (UTI)) - more common to see a. Retrograde movement of going back to kidneys 2. Acquired by hematogenous spread a. Bloodstream (less common) Symptoms ○ Fever** ○ Flank pain ○ Costovertebral angle tenderness ○ Leukocytosis - U/A ○ Pyuria with white cell casts in the urine sediment ○ Positive urine culture ○ Bacteremia - CBC Risk factors are similar to recurrent cystitis ○ Supports the concept of ascent of organisms from the bladder Specific variables (risk factors) ○ Intercourse ○ New sexual partner ○ Spermicidal use ○ Diabetes ○ History of previous UTI ○ Stress incontinence Most common (85%) organism causing acute pyelonephritis is E. Coli** Differential diagnosis of acute pyelonephritis Acute appendicitis (pain in inferior R quadrant, present with fever) Acute salpingitis (inflammation of the fallopian tubes - patients who have used spermicidal, tampons, can appear in either L or R inferior quadrant) Nephrolithiasis (most common - severe pain that starts acute and does not begin with fever) Acute cholecystitis (pain in superior R quadrant) Psoas or paravertebral abscess (½ symptoms, sonogram or CT scan to rule out) Hemorrhagic cyst in polycystic kidney disease (breaks and gives inflammation perform sonogram or CT scan) Acute pancreatitis (comes with fever, vomiting, abdominal pain that radiates to back) Chronic pyelonephritis Recurring inflammation of the kidney Predominant interstitial inflammation with scarring of renal parenchyma and gross deformity of pelvicalyceal system ○ Chronic obstructive pyelonephritis ○ Reflux nephropathy Hematuria (presence of blood in urine) Clinical sign requiring careful evaluation Earliest manifestation of serious underlying processes ○ Renal carcinoma ○ Bladder carcinoma ○ Glomerulonephritis (inflammation of the glomerulus) Classification ○ Gross vs. microscopic Gross: describes a visible change in the color of the urine to red, pink, or brown (can see it) Red or pink urine that = is consistent with a urinary tract source, Brown (tea-colored) translucent = glomerular bleeding Microscopic Commonly discovered by urine dipstick or automated U/A Symptoms Unilateral colicky flank pain = nephrolithiasis Discovered unexpectedly (asymptomatic hematuria) such as during screening of a diabetic patient for proteinuria ○ Upper tract vs. lower tract Upper tract Damage to the glomerular endothelium as in vasculitis and crescentic glomerulonephritides, can permit passage of RBCs into the urine Change in the structure of the basement membrane may allow RBC passage into the urine ○ Alport’s disease and thin basement membrane disease in which the basement membrane is altered by mutations in its collagen components) Isolated damage to glomerular epithelium rarely produces hematuria Lower tract Nephrolithiasis Urothelial tumors Ascending infection ○ Damage the lining of this transport system with resultant bleeding In men, inflammation of a prostate gland secondary to prostate cancer or infection Blood may enter the urine more distally, as in the case of urethritis or contamination from menses Prevalence less than 1% to 16% Etiology and pathogenesis ○ Blood may enter the urine at any point along the urinary tract ○ Upper tract (kidneys, renal collecting system) ○ Lower tract (ureters, bladder, prostate, urethra) ○ Gross bleeding is often from the lower tract ○ Microscopic hematuria can be more difficult to localize Differential diagnosis Brown colored ○ Glomerular IgA nephropathy (most common primary glomerulonephritis) Post streptococcal glomerulonephritis (2nd most common) Red colored ○ Tubulointerstitial Interstitial nephritis (drug-induced) Sarcoidosis ○ Collecting system Nephrolithiasis ○ Ureters Urothelial cell neoplasms Nephrolithiasis ○ Bladder Transitional cell carcinoma ○ Urethra Urethritis ○ Male-specific Prostate cancer Prostatitis Benign prostatic hyperplasia ○ Female-specific Endometriosis Menstrual contamination ○ Vascular Renal artery thrombosis with infarction ○ Nonspecific Strenuous exercise Sexual intercourse Optimum Treatment Determined by the underlying cause For glomerular disease or polycystic kidney disease ○ Refer to nephrologist Progressive renal insufficiency in the setting of glomerular disease warrants urgent referral for consideration of a renal biopsy Referral to a urologist should be made for those with gross hematuria, an identified mass, or persistent hematuria, and those at high risk for malignancy Azotemia Increased levels of urea (BUN), creatinine, waste products and nitrogen compounds that are not cleased/elminated/filtered bby the kidneys Classification ○ Pre-renal azotemia: the blood supply to the kidneys is inadequate ○ Post-renal azotemia: the urinary outflow tract is obstructed Other causes ○ Congestive heart failure ○ Shock ○ Severe burns ○ Prolonged vomiting or diarrhea Increased Blood Urea Nitrogen (BUN) Urea nitrogen is what forms when protein breaks down Pre-renal ○ Acute and chronic intrinsic renal disease ○ Decreased effective blood volume with decreased perfusion Post-renal ○ Obstruction of urine flow ○ High protein intake states Decreased BUN High carbohydrate/low protein diets Increased anabolic demand ○ Pregnancy ○ Infancy ○ Acromegaly Malabsorption states Severe liver damage Increase Serum Creatinine Creatinine is a waste product that forms when creatinine breaks down Creatinine is a substance found in muscle Creatinine levels help determine kidneys function Renal functional impairment Creatinine clearance is significantly reduced before any rise in serum creatinine occurs Instrinsic renal lesions, decreased perfusion of the kidney, obstruction of the lower urinary tract Glomerular disorders Primary vs Secondary ○ Immune mechanisms underlie most of them ○ Antibody associated injury: 1. Deposition of soluble circulating antibodies 2. Antibodies reacting in-situ Circulating immune complexes Kidney act as “innocent bystander” since Ag are NOT from renal origin ○ Endogneous - SLE ○ Exogenous - post-streptococcal The Ag-Ab complexes are trapped in glomeruli producing injury through complemet binding Immunefluorescence stain gives a granular appearance In Situ Antibodies Anti GBM (glomerular basement membrane) nephritis in which Ab are directed against fixed Ag Occurs 3.5 gm/day) 2. Generalized edema (anasarca) (retention of salt and water) 3. Hypoalbuminemia (loss of volume with compensatory Aldosterone secretion) ○ ○ 4. Hyperlipidemia and lipiduria Etiology: Children under 15 y/o Primary renal disease * Lipoid nephrosis “minimal change disease” Adults - more often related with systemic diseases (DM, SLE, and amyloidosis as membranous GN) Acute nephritic syndrome Glomerular syndrome characterized by ○ Visible hematuria ○ Mild to moderate proteinuria ○ Hypertension (acute post streptococcal GN) Nephrotic syndrome ○ Proteinuria (>3.5 gm/day) ○ Hypoalbuminemia ○ Edema ○ Hyperlipidemia ○ Lipiduria ○ Nephrotic syndrome involves loss of a lot of protein ○ Nephritic syndrome involves loss of a lot of blood Glomerulonephritis Disease characterized by alteration in GBM with proliferation of glomerular cells Type I lesions (75% of cases) ○ Eg. Good Pasteur Syndrome ○ There are subendothelial linear deposit of dense bodies Type II lesions (25% of cases) ○ Eg. post strep. SLE, IgA nephropathy) ○ There is intramembranous granular “lumpy bumpy” deposit of dense bodies Glomerular diseases Common cause of hematuria in children, only in 5% in adults Must be considered in any patient with hematuria and renal insuffiency may be rapidly progressive and advances quickly to end-stage renal disease needing dialysis Isolated glomerular hematuria in absence of proteinuria or renal insufficiency in an adult is most commonly caused by immunoglobulin A nephropathy, Alport’s syndrome (i.e., hereditary nephritis), or thin basement membrane disease Urinary tract malignancies Accounts for up to 15% of cases, 75% are associated with bladder cancer Rare in patients females Rate of formation affected by ○ Genetic ○ Nutritional ○ Environmental factors Relative risk for nephrolithiasis for patients with a positive family history may be as great as 2.5% Prevalence has risen over the past 20 years from 3.2% to 5.2%. In the US, prevalence is greatest among those who live in the southern latitudes Calcium stones 75-80% calcium Calcium oxalate alone or combined with calcium phosphate Calcium oxalate stones ○ Brown or gray colored ○ Small and well circumscribed ○ Microscopic crystals are dumbbell or pyramid shape Calcium phosphate stones ○ Beige or white ○ Form apatite and brushite crystals Other ○ Uric acid stones (5-10%) ○ Struvite stones (10-15%) ○ Cystine stones (2%) Hypercalciruria Most common metabolic disorder in people whom stones develop, affects 50% of patients Classification: absorptive, renal leak, hormonal Absorptive hypercalciuria Most common cause of abnormal calcium excretion Patients tend to absorb and excrete a higher proportion of dietary calcium Familial disease Renal leak Renal hypercalciuria is a syndrome of inappropriate renal wasting of calcium which leads to the stimulation of parathyroid hormone and vitamin D in efforts to normalize the serum calcium Hormonal hypercalciuria Develops in hyperparathyroidism both primary and paraneoplastic origin Granulomatous disorders as sarcoidosis may also lead to hypercalciuria due to increased levels of vitamin D Clinical presentation ○ Renal colic caused by an acute obsrutction of the urinary tract ○ Severe pain begins suddenly in the flank and radiates laterally around the abdomen to the groin, testicles, or labia ○ Urinary frequency and dysuria mayoccur when the stone reaches the ureterovesicular junction ○ Nausea and vomiting are common ○ Microscopic hematuria (75%) ○ Gross hematuria ( reveals all types of stones ○ Asses the presence of obstruction U/A - amorphous crystals CT scan has become the standard radiologic test for evaluating patients with acute renal colic Ultrasonography may still be the preferred imaging choice in children Once a diagnosis of nephrolithiasis has been made, an evaluation should be performed In the acute phase Goal of management ○ Relieve pain ○ Treat infection ○ Determine size, location, presence of obstruction ○ Facilitate stone passage Most ureteral stones 4 mm in diameter or smaller pass spontaneously Larger ones may require: lithotripsy, ureteroscopic removal, percutaneous nephrolithotomy Renal failure Sudden deterioration of renal functions ○ Acute - reversible ○ Chronic - irreversible Azotemia > serum BUN Creatinine levels Acute tubular necrosis Reversible clinical entity Characterized by destruction of tubular epithelium Accompanied by renal failure It is the most common cause of acute renal failure End Stage Renal Disease (ESRD) 4 major causes ○ DM (Primarily type 2) ○ Hypertension ○ Glomerulonephritis ○ Cystic renal disease Neoplasia: 3 questions Characteristics of anaplasia, dysplasia, and metaplasia ○ Dysplasia: disorderly proliferation (non-neoplastic), abnormal growth of epithelial cells Loss of cellular uniformity and orientation They show pleomorphism, hyperchromasia, increased mitosis and loss of polarity Grading depends on the organ 2 levels ○ Low grade - earliest form of a pre-cancerous lesion ○ High grade - carcinoma in situ, transformation into cancer is high, still treatment is effective 3 levels: mild, moderate, severe Higher grades more likely to turn into cancer ○ Invasive caracinoma Remember, dysplasia is a change in the normal shape, size, and organization usually a response to chronic irritation (e.g, smoking) Changes are reversible if stimulus is removed, otherwise, cells will become metaplastic (W/IN A TISSUE OR ORGAN) ○ Anaplasia: a reversal in differentiation or loss of structural and functional differentiation of normal cells. These cell changes are not reversible in nature. It is a characteristic of cancerous tumors “To form backward” - lack of differentiation Exhibit advanced cellular pleomorphism - variation in size and shape of cells There is increased mitotic activity, loss of cell orientation, lack of normal organization in the anaplastic tissue Malignant neoplasms are composed of cells that are pleomorphic and anaplastic ○ Metaplasia: a change in the cell type Ciliated columnar epithelium of the respiratory surface becoming stratified squamous epithelium after prolonged irritation from smoking Changes are also reversible if stimulus is removed, otherwise, cells become anaplastic Invasive and in situ carcinoma characteristics ○ Invasive carcinoma: Penetrates the epithelial basement membrane to invade the tissue Can grow quickly and have irregular borders ○ In situ carcinoma: an intraepithelial malignancy in which malignant cells involve the entire thickness of the epithelium without penetration of the basement membrane Only applies to epithelial neoplasms Tumor suppressor genes ○ Encodes a protein that acts to regulate cell division Promotes apoptosis Prevent DNA damage ○ When a tumor suppressor gene is inactivated by a mutation, the protein it encodes is not produced or does not function properly, and uncontrolled cell division may occur ○ Such mutations may contribute to the development of a cancer Blood cell diseases: 5 questions Hodgkin vs Non-Hodgkin Lymphomas characteristics ○ Hodgkin Lymphoma: malignant lymphoma that is typically of B-cell origin Epidemiology: two peaks Young adults 15-30, older 50-70 Etiology: immunosuppression (e.g., HIV, EBV infection, autoimmune diseases) Clinical features: Adenopathy (painless) - localized above the diaphragm Contiguous spread Lymph nodes in upper portion of the body (neck, underarms, or chest) B symptoms (fever, night sweats, decrease weight) Pruritus: focal or generalized Usually no hepatosplenomegaly (rare but might occur if the spleen or liver are involved) No leukemic phase Currently, more curable than non-Hodgkin Develops at a single site and spreads in a predictable fashion to contiguous lymph node groups For this reason, early in its course, local therapy may be indicated One of the most common forms of malignancy in young adults** Average age at diagnosis of 32 years Rare under 5 years of age; in children under age 10, it is more common in boys than girls Reed Sternberg cell **** characteristic histologic findin (owl eyes nuclei) Chemotherapy: ABVD, BEACOPP ○ Non-Hodgkin Lymphoma: classification based on: Cell type: precursor cells (B cell, T cells) or mature cells (natural killer cells) Location (nodal or extranodal) Tumor grade Adenopathy + Extranodal (multiple lymph node groups) Lymph nodes throughout the body, but can also arise in normal organs Noncontiguous spread Epidemiology: increases with age (peak > 50 years) Etiology: Infections (HIV, EN, HTLV-1, HCV, H. Pylori) Autoimmune diseases (e.g., Hashimoto thyroiditis, rheumatic disease Chromosomal translocation (abnormalitis) Clinical features: Nodal disease: B symptoms (20-50%) ○ Lymphadenopathy, mass, hepatosplenomegaly, cytopenias (decrease RBC, WBC, platelets) Extranodal disease: ○ GI 15% inflammation can evolve to ulcer and perforation of stomach or small intestine Liver/spleen - diffuse hepatosplenomegaly ○ Skin- rash ○ Bone- pathologic features (pain-swelling) ○ CNS- epidural SCC, peripheral nerve infiltration, CNS lymphoma (1%) In children (more frequently between the ages of 10-20) Small noncleaved cell lymphoma ○ Burkitt’s and Non-Burkitt’s: B-cell origin 40-50% of childhood NHLs Lymphoblastic ○ Predominantly B-cell origin, sometimes is hard to distinguish from leukemia; 30% of childhood NHLs Large cell lymphoma ○ Both T and B; 20-25% of childhood NHLs In adults B-cells (more common) ○ 20% Diffuse Large B Cell Lymphoma of all NHL and 60% to 70% of aggressive lymphoid neoplasms Prognosis measured in months ○ 45% follicular Most common form of NHL in the US Is a middle age disease and afflicts males and females equally Usually indolent Prognosis measured in years (7-9%) ○ 10% marginal zone Mucosal sites Driven by chronic antigen stimulation (inflammation) as Sjogren’s, HCV, H. Pylori T-cells (less common) ○ 65 yr have gallstones ○ Complications Cholecystitis Biliary tract obstruction (choledocholithiasis) Infection (chalangitis) Pancreatitis ○ Diagnosis Ultrasonography ○ Treatment If cholelithiasis causes symptoms or complications, cholecystectomy is necessary ○ Risk factors Female sex Obesity (fat) Family history Fortices Increased age (60 y/o or older) American Indian ethnicity Western diet Familial adenomatous polyposis ○ An autosomal dominant inherited condition ○ Characterized by the development of multiple polyps in the intestine ○ Polyps are initially benign, almost all patients will eventually develop colorectal cancer if left untreated ○ Overall, FAP accounts for only ~1% of all cases of colorectal cancer ○ Ocular manifestation: hypertrophy of the RPE (in 90% patients) ○ Respiratory system: 5 questions Cardiac system: 5 questions