Path 2 Quiz 2

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Path 2 Quiz 2
2010-08-19 06:28:24

Path 2 quiz 2 (midterm)
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  1. Nephrotic syndrome characterized by:
    • Proteinuria
    • Hypoalbumemia
    • Generalized edema
    • Hyperlipidemia & lipiduria
  2. Proteinuria due to nephrotic syndrome
    • The glomerulus becomes permeable to albumin
    • Normally there is no protein in the urine
    • 55% of blood proteins are albumin, whose main fxn is to prevent fluid loss by maintaining oncotic/colloid osmotic pressure
  3. Hypoalbuminemia due to nephrotic syndrome
    • Decreased concentration of blood albumin causes the fluid portion of blood to move out of the vessels & into the tissues-> leads to edema
    • The excretion of proteins in the urine (proteinuria) causes there to be less albumins in the blood (hypoalbuminemia) NOT the other way around
  4. Generalized edema due to nephrotic syndrome
    • Puffy looking people
    • Pedal edema- pitted swelling in the lumbars, feet/legs, & body cavities
    • Caused by hypoalbuminemia since there are less proteins to help maintain blood oncotic pressure
  5. Hyperlipidemia & Lipiduria due to nephrotic syndrome
    • Lipoproteins are made in the liver w/ less protein & more fat than usual (due to hypoalbuinemia), & these lipoproteins eventually spill into the urine b/c the glomerulus is permeable to the protein
    • Lipid casts are also present in urine
  6. Causes of nephrotic syndrome
    • Primary Glomerular Disease
    • Systemic diseases: diabetes mellitus (glomerular lesions, renal vascular lesions, pyelonephritis), amyloidosis
  7. Primary Glomerular disease
    • Associated w/ younger people
    • Minimal change disease (lipid nephrosis)
    • *Membranous GMN
    • *Focal segmental glomerulosclerosis- most dangerous, most common cause of chronic GMN of all the nephrotic syndrome disorders
    • *Membranoproliferative GMN

    *all of these diseases can lead to chronic GMN; this list also includes post strep GMN (least dangerous of all diseases) & rapidly progressive GMN (most dangerous of all diseases)
  8. Diabetes Mellitus (Diabetic neuropathy)
    • Glomerular lesions- thickening of the glomerular basement membrane
    • Diffuse glomerulosclerosis
    • Nodular glomerulusclerosis- Kimmel-Wilson lesions (ball like deposits within the mesangial cells)
    • Renal vascular lesions
    • Hyaline arteriosclerosis of both afferent & efferent arterioles
    • Atherosclerosis
    • Pyelonephritis- often w/ necrotizing papillitis b/c of the sweet urine (glucose serves as food for bacteria)
  9. Amyloidosis
    • Intracellular deposition of AA protein in the kidneys, heart, & liver
    • Is incurable & leads to pressure atrophy
  10. Disorders of the tubules & interstitial tissue
    • Acute cystitis
    • Acute pyelonephritis
  11. Acute cystitis
    • The first step for spread of infection to other areas of the urinary tract
    • Common in women
    • Predicting factor for pyelonephritis (1st step)
  12. Acute pyelonephritis
    • Supperative infection of the kidney pelvis & parenchyma
    • Spread of infection can be from the blader to the kidney (MC), from the blood, or from the lymph fluid
    • Caused by gram (-) rods of the intestinal flora, predominantly E coli
    • E coli is the #1 cause of acute cystitis & pyelonephritis
  13. Signs & symptoms of acute pyelonephritis
    • High fever & chills
    • Pain in thoracolumbar area
    • (+) murphy's punch
    • UA will contain bacteria, leukocytes (neutrophils), & WBC casts
    • Necrotizing papillitis= necrosis of kidney pyramids-> hemorrhages-> hematuria (more common with diabetes mellitus)
    • Treatment is w/ antibiotics/uroseptics
  14. GI Tract disorders
    • Erosions
    • Peptic ulcers
    • Achalasia
    • Hiatal hernia
    • Hiatal paraesophageal hernia
    • Zenker diverticulum
    • Mid-esophageal diverticulum
    • Epiphrenic diverticulum
    • Mallory Weiss syndrome
    • Barret esophagus
    • Zollinger Ellison syndrome
  15. Erosions
    • Superficial damage of the GI tract wall
    • Tend to be multiple
    • Recovery time is fast (few days)
  16. Peptic ulcer
    • Deep penetration extending thru the muscularis mucosa & into the submucosal layers
    • 1-2cm
    • Tend to be solitary
    • Recovery time is much longer (weeks/months)
  17. 2 key factors of peptic ulcers
    • Presence of H pylori bacteria
    • Exposure of ulcer to stomach pepsin & acidity (HCl)
  18. 3 organs peptic ulcers develop in
    • Stomach (20%)- H pylori is present in 70% of cases; majority of stomach ulcers found in the lesser curvature
    • Duodenum (80%)- MC; H pylori present in 100% of cases; duodenal bulb is the MC (most proximal, most susceptible) area for ulcers in the entire body
    • Esophageal- very rare
  19. Defensive forces of stomach against peptic ulcers
    • Surface mucous secretions
    • Mucous barrier- alkaline environment produced by bicarbonate secretions (protects against stomach acidity)
    • Mucosal blood flow- most important factor (the vessels are sensitive to vasoconstrictors (nicotine) which make the barrier weaker by reducing blood flow to the area; increased stress-> increased sympathetic constriction-> increased chance for ulcer formation
    • Apical surface membrane transport
    • Epithelial regeneration capacity- regeneration occurs very quickly
    • Elaboration of prostaglandins- prostaglandins suppress the production of gastrin by G cells-> the gastrin stimulation for HCL is then diminished resulting in a decrease of acidity
  20. Aggravating causes of stomach ulcers
    • NSAID's & aspirin- destroy prostaglandins
    • Cigarettes
    • Alcohol
    • H pylori infection
    • Impaired regulation of acid-pepsin secretion
  21. Complications of stomach ulcers
    • Hemorrhage (30%)- MC; vomitting (black coffee w/ milk appearance)- heamatamesis; black stool- melena (the color is black due to reaction b/w iron/heme)
    • Ulcer perforation- may cause peritonitis (operation no matter what)
    • Accumulation of gas under the right side of the diaphragm- due to escaped gas from a complete perforation of the stomach
    • Penetration of ulcer into adjacent organs (pancreas)
    • Pyloric stenosis- caused when scar tissue replaces damaged tissue
    • Transformation into cancer- of the stomach peptic ulcer only; never occurs in the duodenum
    • Hour glass stomach- result of ulcer healing
  22. Hypertophic pyloric stenosis
    Congenital pathology of the newborn where the pyloric muscle is very thick-> decreased lumen size-> milk accumulates in the baby's stomach-> vomiting-> convulsions due to a loss of chloride (1:300)
  23. Diagnosis of gastric pain
    • How long after your meal does your stomach pain begin?
    • 1/2-1 h= stomach peptic ulcer
    • 1-3 h= duodenal peptic ulcer
    • very shortly after meal= stomach cancer
  24. Achalasia
    failure of contraction of the lower esophageal sphincter
  25. 3 major findings of achalasia
    • Asperistalsis
    • Incomplete/partial relaxation of the lower esophageal sphincter
    • Contraction/spasm of the LES
    • All prevent food passage
  26. Neurological problems associated w/ achalasia
    Stem from vagus nerve & ganglion & myenteric plexus
  27. Chaga's disease
    • Caused by trypanosoma cruzi & damages the myenteric plexus
    • Is one of many orders that results in achalasia
  28. Signs & symptoms of achalasia
    • Dysphagia- abnormal swallowing
    • Regurgitation
    • Predisposition to esophageal adenocarcinoma
  29. Hiatal hernia
    • aka diaphragmatic hernia
    • Separation of diaphragmatic crura & widening of the space b/w the muscular crura & the esophageal wall
  30. Hiatal paraesophageal hernia
    aka rolling hernia-> part of the stomach bulges through in an opening near the esophagus-> compression of venous blood flow by diaphragm-> venous infarction-> wet gangrene
  31. Zenker diverticulum
    • Close to upper esophageal sphincter
    • Cause of aspiration pneumonia
    • No dysphagia, just regurgitation
  32. Mid-esophageal diverticulum
    In the middle of the esophagus, caused by pulling of the esophageal wall by developing scar tissue from lymphadenitis of paratracheal/esophageal lymph nodes
  33. Epiphrenic diverticulum
    • Above the lower esophageal sphincter
    • Aspiration pneumonia
    • Regurgitation
  34. Mallory Weiss syndrome
    • Irritation of the distal esophagus due to prolonged vomiting
    • Common in alcoholics
    • aka laceration
    • Bleeding/hemorrhage in 10% of cases
    • Rupture of the esophagus leads to death
  35. Barret Esophagus
    • Replacement of normal distal stratified mucous squamous epithelia by metaplastic columnar epithelia that have goblet cells
    • Prolonged heart burn
    • Drinking baking soda can help
    • Increases the chance of esophageal cancer
  36. Zollinger Ellison syndrome
    • Hypersecretion of gastrin by gastrin producing tumors known as gastrinomas
    • Benign tumors of the pancreas, duodenum, or peri-pancreatic tissue
    • Benign because tumor cells are normal
    • Increased gastrin leads to increased HCl-> peptic ulcers in the stomach, duodenum, & jejunum
    • Malignant b/c tumors can metastasize to the liver-> death from hepatic failure
    • Manifested by diarrhea in 50% of cases
  37. Rheumatic fever
    • Affects mostly teenagers
    • Marked by swelling of the palantine tonsils (tonsilitis)
    • Is indirectly caused by beta hemolytic strep group A- antibodies attach to heart & destroy tissue-> Molecular mimicry theory
    • Develops in repeated strep throat episodes
  38. Signs & symptoms of rheumatic fever
    • Migratory arthritis of the middle sized jts
    • Rash
    • Sydenham's cholera- rare but obvious sign of RF characterized by jerky, involuntary movements of the facial muscles & extremities
  39. Rheumatic fevers effect on the heart
    • Aschoff's nodules- pathogenic for rheumatic myocarditis- fibronoid necrosis in autoimmune diseases
    • Pericarditis (10-15% of cases)- formation of connective tissue fibers b/w visceral & parietal layers of pericardium
    • Endocarditis (80% of cases)- inflammation of the cusps of the heart valves
  40. Order of valvular involvement of endocarditis
    • Mitral valve (stenosis)
    • Aortic valve (stenosis)
    • Tricuspid valve
    • Pulmonary valve
  41. Mitral valve stenosis
    • Inflammation-> healing-> scar tissue causing partial closure of valve-> regurgitation or valve insufficiency
    • Causes a back up of blood in the LA & pooling of blood in the lungs
    • LA must work harder-> hypertrophy
    • Increased blood hydrostatic pressure in LA leads to congestive heart failure, & enlarged LA may compress bronchi
    • Esophagus deviates from its normally straight path to stomach
    • Potential for thrombus development from slowing of blood-> infarction
  42. Aortic valve stenosis
    • Causes left ventricular hypertrophy which can lead to heart failure
    • Other causes of aortic insufficiency: bacterial endocarditis, tertiary syphilis, RA
    • Decreased diastolic pressure
    • Demussette's sign