Path 2 Quiz 2

• Proteinuria
• Hypoalbumemia
• Generalized edema
• Hyperlipidemia & lipiduria

• 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

• 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

• 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

• 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

• Primary Glomerular Disease
• Systemic diseases: diabetes mellitus (glomerular lesions, renal vascular lesions, pyelonephritis), amyloidosis

• 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)

• 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)

• Intracellular deposition of AA protein in the kidneys, heart, & liver
• Is incurable & leads to pressure atrophy

• Acute cystitis
• Acute pyelonephritis

• The first step for spread of infection to other areas of the urinary tract
• Common in women
• Predicting factor for pyelonephritis (1st step)

• 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

• 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

• Erosions
• Peptic ulcers
• Achalasia
• Hiatal hernia
• Hiatal paraesophageal hernia
• Zenker diverticulum
• Mid-esophageal diverticulum
• Epiphrenic diverticulum
• Mallory Weiss syndrome
• Barret esophagus
• Zollinger Ellison syndrome

• Superficial damage of the GI tract wall
• Tend to be multiple
• Recovery time is fast (few days)

• Deep penetration extending thru the muscularis mucosa & into the submucosal layers
• 1-2cm
• Tend to be solitary
• Recovery time is much longer (weeks/months)

• Presence of H pylori bacteria
• Exposure of ulcer to stomach pepsin & acidity (HCl)

• 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

• 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

• NSAID's & aspirin- destroy prostaglandins
• Cigarettes
• Alcohol
• H pylori infection
• Impaired regulation of acid-pepsin secretion

• 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

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)

• 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

failure of contraction of the lower esophageal sphincter

• Asperistalsis
• Incomplete/partial relaxation of the lower esophageal sphincter
• Contraction/spasm of the LES
• All prevent food passage

Stem from vagus nerve & ganglion & myenteric plexus

• Caused by trypanosoma cruzi & damages the myenteric plexus
• Is one of many orders that results in achalasia

• Dysphagia- abnormal swallowing
• Regurgitation
• Predisposition to esophageal adenocarcinoma

• aka diaphragmatic hernia
• Separation of diaphragmatic crura & widening of the space b/w the muscular crura & the esophageal wall

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

• Close to upper esophageal sphincter
• Cause of aspiration pneumonia
• No dysphagia, just regurgitation

In the middle of the esophagus, caused by pulling of the esophageal wall by developing scar tissue from lymphadenitis of paratracheal/esophageal lymph nodes

• Above the lower esophageal sphincter
• Aspiration pneumonia
• Regurgitation

• 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

• 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

• 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

• 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

• 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

• 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

• Mitral valve (stenosis)
• Aortic valve (stenosis)
• Tricuspid valve
• Pulmonary valve

• 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

• 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