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110 Cards in this Set
- Front
- Back
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Understand the mechanism of H pylori in causing ulcers
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H. pylori - infectious agent that thrives in acid environment and destroy mucosal carrier that protects stomach from harmful effects of its digestive enzyme
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signs and symptoms of ulcers
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Pain (burning, gnawing, cramp-like, rhythmic, empty stomach 1-2am)
Location of pain: midline in epigastruim near xiphoid, below costal margin, back, sometimes right shoulder |
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definition of GERD
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backward movement of gastric contents into the esophagus
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GERD, who is susceptible
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obese because of meals high in fat.
also infants and children children w/ cerebral palsy, Down syndrome, and other neurologic disorder Reflux is commonly corrected w/ age Symptoms subside in most children by 2 years of age |
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complications GERD
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• Complications w/ perisitent reflux:
o Esophagitis o Cycle of mucosal damage that causes hyperemia, edema, and erosion of the luminal surface o Barrett esophagus Increased risk for development of esophageal cancer Strictures (caused by scar tissue, spasm, edema) |
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causes of bowel obstruction
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o Mechanical (intrinsic or extrinsic)
External hernia Postoperative adhesions Strictures Tumor Foreign bodies Intussusceptions: telescoping of bowel into the adjacent segment - movement of one segment of colon into another • Most common in children under 2 years of age • Most common site: terminal ileum into right colon Volvulus: complete twisting of the bowel on an axis formed by its mesentery o Paralytic: obstruction results from neurogenic or muscular impairment of peristalsis Abdominal surgery (most common is paralytic ileus) Inflammatory conditions Intestinal ischemia Pelvic fractures Back injuries |
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Understand diverticular disease
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Mucosal layer of the colon herniates through the muscularis layer often in sigmoid colon
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how diverticular disease diagnose
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barium enema x-rays studies
CT scans Flat abdominal radiographs |
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mechanism of diarrhea
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excessively frequent passage of stools by bowel irritation, inability to absorb certain fluid i.e. milk, or release of endotoxins by bacteria that stimulate fluid secretion, or infectious agents destroy intestinal epithileal cells
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Causes of diarrhea
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• Large-volume diarrhea Osmotic diarrhea
• Saline cathartics • Lactase deficiency (magnesium from milk of magnesia are poorly absorbed) Secretary diarrhea • Acute infectious diarrhea o Vibrio cholerae, E. coli, rotavirus that secrete toxins that simulate fluid secretion o Shigella, Salmonella, Yersinia, Campylocbacter that destroy intestinal epithelia cells (continuous absorption) • Failure to absorb bile salts • Fat malabsorption • Chronic laxative abuse • Carcinoid syndrome • Zollinger-Ellison syndrome • Fecal impaction • Small-volume diarrhea : Inflammatory bowel disease • Crohn disease • Ulcerative colitis Infectious disease • Shigellosis • Salmonellosis Irritable colon |
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Treatment of diarrhea
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replacement of fluids and electrolytes, oral replacement therapy (ORT)
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cirrhosis stages
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i think this is the alcoholic liver stage
o Stage 1: fatty changes with fatty liver Steatosis: accumulation of fat in hepatocytes Liver becomes yellow & enlarged Do not produce symptoms Reversible after alcohol is discontinued o Stage 2: Alcoholic hepatitis Inflammation & necrosis of liver cells (always serious and sometimes fatal) S&S: hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites, and liver failure (could also be asymptomatic) o Stage 3: Alcoholic cirrhosis S&S: fine, uniform nodules on liver surface • Regeneration causes nodules to become larger & irregular => hepatic back flow to esophagus • Formation of new portal tracts and hepatic veins -> portal hypertension, extrahepatic portosystemic shunts, and cholestasis |
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foods which must be avoided in celiac disease
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gluten-containing grains (wheat, barley, rye or oat)
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cause of malabsorbtion
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3 Causes : + intraluminal maldigestion – nutrients are not processed in the intestinal lumen
i.e. pancreatic insufficiency, hepatobiliary disease, intraluminal bact. Growth + disorders of transepithelial transport – impair uptake and transport of intraluminal nutrients across the mucosal surface of intestine i.e. celiac disease and Crohn’s diease + lymphatic obstruction – affect fat digestion to systemic circulation i.e. congenital defects, neoplasms, trauma, and some infectious disease |
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Understand basic differences among types of hepatitis and which one does not produce carriers
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basic differences : please look at study guide
Hep A and E does not produce carriers |
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causes of gallstone formation
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obesity
women who have multiple pregnancies or taking oral contraceptives women overweight over 40/60 (I’m not sure if it’s 40 or 60), multiple pregnancy => excrete more hormones, genetic (alcoholism) (cause of cholecystitis) |
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What is gallstones ?
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precipitation of substances contained in bile , mainly cholesterol, others are calcium salts with bilirubin.
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type of pain in cholecystitis
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Acute cholecystitis pain become more severe in right upper quadrant, right subcostal region is tender, muscles surrounding the area spasm
• Chronic cholecystitis colicky pain w/obstruction of biliaryflow |
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Know causes of acute pancreatitis
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• Acute pancreatitis
gallstone, alcohol abuse + Alcohol => potent stimulator of pancreatic secretions, cause spasm and partial obstruction of sphincter of pancreatic duct |
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Understand the mechanism of seizures
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Abnormal, uncontrolled electrical discharge from a group of neurons in cerebral cortex
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Understand spinal shock
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Acute Spinal Cord Injury
- What is it? → damage to the neural elements - Causes : direct trauma i.e. penetrating wounds, fractures, dislocation, subluxations → contused cord at the site of injury + above + below → loss of blood flow → infarction → complete loss of motor, sensory, reflex, autonomic function BELOW the site of injury (remember that the manifestations are effective below the site of injury) Which is called SPINAL CORD SHOCK |
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Manifestations of spinal shock
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flaccid paralysis
loss of tendon reflexes absence of somatic and visceral sensations loss of bowel and bladder function loss of systemic sympathetic vasomotor TONE → vasodilatation, increased venous capacity, hypotension |
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PATHOPHYSIOLOGY of spinal shock
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1. Primary neurologic injury – at the time of injury , irreversible
Small hemorrhage in the gray matter of the cord → edema → necrosis 2. Secondary injuries – follow primary, promote the SPREAD of injury 3 things that happen: + Vascular trauma and hemorrhage → vascular damage → form lesions → ischemia , increased vascular permeability, edema + Loss of vasomotor tone and neural reflexes below the injury → blood flow compromise + Release of • vasoactive substances ( i.e. norepiepherine, serotonin, dopamine, histamine) → cause vasospasm → decreased blood flow → necrosis • cellular enzymes ( i.e. proteolytic and lipolytic) from injured cells → delayed swelling, demyelination, and necrosis ALL 3 THINGS lead to TISSUE DESTRUCTION!!! |
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autonomic hyperreflexia
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acute episode of exaggerated sympathetic reflex response
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manifestations of autonomic hyperreflexia
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MANIFESTATIONS
+ vasospasm + hypertension from mild to severe + skin pallor, gooseflesh, piloerector vasodilatation + flushed skin, sweating above level of injury, pounding headache + nasal stuffiness + anxiety |
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Treatment of autonomic hyperreflexia
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+ Monitor B/P (why? Hypertension) while REMOVE the cause
+ Position : upright, remove support hose or binders → reduce venous return → decrease B/P + if not resolve – drug that block autonomic function is administered + Finally, prevention of stimuli is necessary |
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causes of autonomic hyperreflexia
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STIMULI – visceral distention i.e. full bladder or rectum
Stimulation of pain receptors i.e. pressure ulcers, ingrown toenails, dressing changes, ALSO diagnostic procedures Visceral contraction i.e. ejaculation, bladder spasms or uterine contractions |
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difference in epidural and subdural hematomas
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Epidural: between bone and Dura related to tear in artery => fast hemorrhage
+ brief unconcious => LUCID period when regain conciousness => then unconcious If not removed => increased ICP and death Subdural : between dura and arachnoid, tear in veins => slow progression, there are 3 categories: acute, subacute, and chronic, also have decrease level of conciousness |
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Coup - Coutrecoup injury
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because brain is floating inside the skull, when there is a force, brain hits the skull then rebound to the opposite site:
+ Coup => direct contusion at the site of force + Coutrecoup => rebound against the inner skull surface |
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mechanism of strokes
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stroke is a vascular disorder => injures brain tissue => acute focal neurologic deficit
2 types : + ischemic: interruption of blood flow in cerebral vessel + hemorrhagic: bleeding into brain tissue |
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which stroke is more fatal
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hemorrhagic
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what typical heart disease in stroke patients
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atrial fibrillation => cardioembolic stroke
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a stroke related to brain injury
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ischemic stroke (can check in brain injury - hypoxia/ischemic brain injury)
I think this is the answer. but im not sure. |
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know the difference between viral and bacterial meningitis.
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Bacteria
+ CSF contains neutrophils, increased serum protein, decreased sugar - Treatment of course is antibiotics ( with corticosteroids) Viral + course is less severe + CSF contains lymphocytes, protein is slightly elevated, sugar is normal (i think because viruses don't love sugar like bacteria do) + because this is viral infection, treatment base on symptoms (symptomatic treatment), also self-limited (not contagious - i guess) |
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Children who are at risk for UTIs are...
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premature infants
children with systemic or immunologic disease children with neurogenic bladder or vesicoureteral reflux family history of UTI girls younger than 5 years of age with history of UTI |
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Characteristics of UTI in children
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involve upper urinary tract (PYELONEPHRITIS) => renal scarring and permanent kidney damage
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S and Sx of UTI in children
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infants : s and sx of sepsis - fever, hypothermia, apneic spells, poor skin perfusion, abd distention, diarrhea, vomiting, lethargy, irritability
+ older infants : feeding problems, failure to thrive, diarrhea, vomiting, fever, foul – smelling urine + toddlers : abd pain, vomiting ,diarrhea, abnormal voiding pattern, foul – smelling urine, fever, and poor growth + older children with lower UTI – enuresis, frequency, dysuria, suprapubic discomfort |
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Etiology of UTI in general
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Bacteria enter urethra ( or bloodstream in neonates and immunosuppressed) then colonize.
Risk : + urinary obstruction and reflux disorders + neurogenic bladder + sexually active women ( use diaphragm or spermicide for contraception) + post menopause women and men with prostate disease + elderly + catheterization + diabetes |
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Etiology of UTI in elderly
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+ immobility → poor bladder emptying
+ prostatic hyperplasia or kidney stones → bladder outflow obstruction + urine retention → bladder ischemia + senile vagintitis, constipation, diminish bactericidal activity of secretions + CATHETERS!!! |
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S and Sx of UTI in elderly
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S and Sx of UTI in elderly - vague
+ urgency, frequency , incontinence + anorexia, fatigue, weakness, change in mental status + upper UTIs (serious ) – S and Sx of infection alter or absent |
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washout phenomenon
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urine washes bacteria out of the urethra
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common treatment for Wilm’s tumor
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surgery, chemo, sometimes radiation
survival rate 80% ^^! |
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Stages of wilm's tumor
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stage I : limited to kidney but capsular surface intact
stage II: tumor can't be excised stage III: extension of tumor to abd stage IV: metastasis - common involve lungs |
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Nephrotic syndrome - pathophysiology
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Glomerular damage → increased permeability to proteins – proteinuria ( >= 3.5g/day)
→ hypoproteinemia → 2 things: + decreased plasma oncotic pressure → edema + compensatory synthesis of proteins by liver → hyperlipidemia |
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S and Sx of nephrotic syndrome
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+ generalized edema → dyspnea, pleural effusions, acites
+ also lost globulins → infection + loss of coagulation and anticoagulation factor → renal vein thrombosis, deep vein thrombosis, pulmonary emboli + hyperlipidemia → atherosclerosis |
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Pyelonephritis
What? |
Inflammation of upper kidney – tubules, insterstitium, renal pelvis
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Pyelonephritis
How many types? |
2 types – acute – caused by bacteria infection such as gram-negative
Chronic – recurrent infection + vesicoureteral reflux |
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Causes of acute pyelonephritis
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catheter, reflux, pregnancy, neurogenic bladder
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S and Sx of acute pyelonephritis
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abrupt onset, chills, fever, headache, back pain, malaise
Dysuria, frequency, urgency |
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Etiology of chronic pyelonephritis
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bacterial infection and reflux or obstructive abnormalities
→ scarring and deformation of renal calices and pelvis → renal failure |
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S and Sx of chronic pyelonephritis
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same as acute, but insidious onset with polyuria, nocturia and mild proteinuria with severe HTN ( because of impending kidney failure)
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Glomerular Nephritic – pathophysiology
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Proliferative inflammatory response of the glomeruli → damage capillary wall → red blood cells into urine → hematuria with red cell casts( coca cola color urine) , absent GFR, azotemia ( nitrogenous waste in blood), oliguria, and HTN
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most common type of renal stone
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calcium stones - 70 - 80 % e.g. calcium oxalate, calcium phosphate or combination of them)
3 other types - magnesium ammonium phosphate, uric acid, and cystine stones |
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signs and symptoms of renal stones
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PAIN!!! 2 types
+ renal colic - pain with stretching of collecting tubules or ureters. it is an intermittent or acute pain, upper outer quadrant of abd on affected side. also cool and clammy skin + noncolicky renal - pain at renal calices or pelvis, a dull, deep ache in flank or back, increase when drinking large amount of fluid |
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clinical manifestation of polycystic kidney disease
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severe renal dysfunction, impaired lung development, liver fibrosis, portal HTN
cardiovascular disorders, cerebral aneurysm, liver cyst, pancreas cyst, subarachnoid hemorrhage, pain, UTI, renal colic by kidney stones => slow and end stage kidney disease |
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Pathophysiology of polycystic kidney disease
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Mutant genes in PKD1 ( chromosome # 16) or/and PKD2 (chromosome # 4)
autosomal recessive |
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Causes if chronic renal failure
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Conditions that cause permanent loss of nephrons such as + diabetes
+ HTN + glomerulonephritis + polycystic kidney disease |
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Stages of chronic renal failure
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Diminished Renal Reserve - insidious (GFR 50% of normal)
=> Renal Insufficiency ( 20-50%) => Renal Failure ( 20-25%) => ESRD (<5%) |
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Manifestations of Chronic Renal Failure
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Fig 25-4 patho book pg 565 chapter 25 : )
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What is pneumonia?
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Inflammation of the alveoli and bronchioles
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Classifications of pneumonia
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+ type of agent : typical or atypical
+ distribution of infection : lobar or bronchopneumonia + setting: community or hospital |
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What is Community – acquired pneumonia?
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Defined as an infection that begins outside the hospital or id diagnosed within 48hrs after admission to the hospital in a person who has not resided in a long-term care facility
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Community – acquired pneumonia common bact. cause?
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S. pneumonia
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What is Hospital – acquired pneumonia?
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Infection of the lower resp. tract within 48 hr or more after admission
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Possible causes of Hospital – acquired pneumonia?
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Mechanical ventilation, endotracheal intubation, tracheotomy
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Hospital – acquired pneumonia common bact. Cause?
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Pseudomonas aeruginosa
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Pathophysiology of typical pneumonia?
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Infection by bacteria that multiply extracellularly in alveoli → cause inflammation → cause exudation of fluid
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What happened in atypical pneumonia?
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Viral or mycoplasma infection of the alveolar septum interstitium
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common bact. Cause of atypical pneumonia?
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Mycoplasma pneumonia
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S and Sx of atypical pneumonia?
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Insidious onset, dry cough, fever, muscle aches, pain, headache
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Pathophysiology of S. pneumonia pneumonia?
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Colonization of organism in the nasopharynx → activate B-cell response however delayed b/o the bact’s capsule → produce antibodies.
If absence of antibodies ( no memory – I think) → spleen kicks in → produce macrophages → elimination of the organisms So… in person with spleen dysfunction i.e sickle cell disease → problem!!! |
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S and Sx of S. pneumonia pneumonia?
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Malaise, fever, chills, cough ( watery sputum), crackles, pleuric pain, in elderlies – loss of appetite and changes in mental status
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Legionnaires Disease???
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Caused by legionella pneumophilla found in warm standing water, a gram negative rod causes bronchopneumonia
Risk factors: smokers, person with chronic disease, impaired cell-mediated immunity S and Sx : diarrhea, hyponatremia, confusion Complications: consolidation of lung tissue, impaired gas exchange |
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Know differences between emphysema and chronic bronchitis
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respiratory responsiveness to hypoxic stimuli
Emphysema: Pink puffers or fighters → able to fight !!! → able to overventilate → proportionate loss of ventilation and perfusion → maintain normal blood gas levels Chronic bronchitis Blue boaters or nonfighters → not able to fight. Why??? → because excessive bronchial secretions → airway obstruction → mismatching of ventilation and perfusion → hypoxemia and cyanosis |
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pathophysiology of chronic bronchitis
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Smoking → stimulate the inflammatory cells → hypertrophy of submucosal gland → hypersecretion of mucus → increased goblet cells and mucus plugging → infection → inflammation→ fibrosis of bronchiolar wall
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pathophysiology of TB
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Inhaled droplet nuclei of Mycobacterium ( M. tuberculosis)
→ Macrophages engulf and present to T cells → T cells stimulate macrophage to release lytic enzymes → the enzymes also damage lung tissue → Also form Ghon focus (tubercle bacilli + modified macrophages + other immune cells) → formation of caseous (cheeselike) granunolas |
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Different types of croup and causes
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+ viral croup – viral infection ( e.g. parainfluenza virus), in children 3 months – 5 yo – affects the upper airway ( laryngotracheal tree)
+ Spasmodic croup – allergic reaction + epiglottitis – viral infection (influenza type B) affect the supraglotic area, children 2-7 yo |
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Special precautions to be taken with epiglottitis
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No lying down, no use of tongue blade b/o risk for cardiopulmonary arrest, no procedure such as draw blood…. Action!!! → immediate establishment of tracheotomy or endotracheal tube
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Special precautions to be taken with viral croup
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no tongue blade or anything that stimulate pharynx, exposure to cold moist air can relieve the symptoms
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S and Sx of G. Barre ?
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progressive muscle weakness of limbs → flaccid paralysis. Affect resp. muscle and ANS. Pain
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G. Barre causes?
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Linked to infection with virus like EBV and mycoplasma because of antibodies attack nerve gangliosides
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Guillain-Barre syndrome!!! What?
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Acute immune-mediated polyneuropathy. Polyneuropathy is the demyelination or axonal degeneration of multiple peripheral nerves
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S and Sx of M. Gravis?
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Muscle weakness (common eye and preorbital muscle), fatigue then progressed generalized weakness. Also – myasthenia crisis: sudden muscle weakness→ alter ventilation most often when stress, infection…
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Pathophysiology of M.Gravis?
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autoimmune disease: antibody – mediated destruction of acetylcholine receptors
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Myasthenia Gravis!!! What?
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Disorder of transmission at the neuromuscular junction → affect communication between motor neuron and innervated muscle cell
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S and Sx of duchenne muscular atrophy
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2-3 yo child frequent falls, abnormal posture, scoliosis, contractures, about 7-12 need wheelchairs. Forming pseudohypertrophy – increase muscle size from connective tissue infiltration
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Pathophysiology of Duchenne muscular dystrophy?
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Defective form of protein dystrophin → fails to provide normal attachment site for contractile proteins → necrosis of muscle fibers
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Muscle atrophy!!!! What?
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Degeneration and necrosis of skeletal muscle fiber – genetic disorders → replace with fat and connective tissue
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S and Sx of parkinson
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tremor!!!!, rigidity, bradykinesia – sudden slow movements, involuntary movement, abnormal gait, dementia
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Causes of Parkinson
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drug induced such as antipsychotic
Genetic – inherited alpha-synuclein and parkin genes |
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Pathophysiology? Of Parkinson
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Progressive destruction of the nigrostriatal pathway with reduction striatal dopamine concertrantion
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What is Parkinson?
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Degenerative disorder of basal ganglia
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S and Sx of ALS
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weakness, spasticity, impaired fine motor control – death… from cranial nerve involvement and resp. muscle
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Pathophysiology of ALS
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mutations of SOD1 on #21 which prevent free radical formation
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Causes of Parkinson
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drug induced such as antipsychotic
Genetic – inherited alpha-synuclein and parkin genes |
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Pathophysiology? Of Parkinson
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Progressive destruction of the nigrostriatal pathway with reduction striatal dopamine concertrantion
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What is Parkinson?
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Degenerative disorder of basal ganglia
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S and Sx of ALS
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weakness, spasticity, impaired fine motor control – death… from cranial nerve involvement and resp. muscle
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Pathophysiology of ALS
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mutations of SOD1 on #21 which prevent free radical formation
affect motor neurons in anterior horn cells (LMNs) of the spinal cord, motor nuclei of brain stem, UMNs of cerebral cortex → shrinkage of musculature and muscle fiber atrophy – amyptrophy |
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S and Sx of m. sclerosis
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problem with coordination, paresthesia, fatigue
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Pathophysiology of m. sclerosis
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Immune-mediated disorder : T-cells and macrophages and antibody → damage myelin forming oligodendrocytes protein
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MSclerosis what?
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demyelinating disease of CNS→ neurologic dysfunction – young and middle aged adults 20-45 yo – Risk factor : familial aggregation of the disease
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pathophysiology of ARDS
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Accumulation of neutrophils → increase inflammatory response → alveolar cell damage
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Effect of resp. failure
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Impaired perfusion → hypoxemia without hypercapnia
Hypoventilation |
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effect of respiratory failure and effect of elevated CO2
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elevated CO2 → cause vasodilation → cause headache
→ increased CSF fluid pressure → papilledema |
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causes of atelectasis
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Obstruction caused by mucus plug, tumor mass. Increase after surgery
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what causes BPD?
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Mechanical ventilation → high inspired oxygen concentration and injury from positive – pressure ventilation
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What is resp. distress syndrome?
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Premature neonates
→ surfactant deficiency → irregular lung infiltration → + atelectasis + increased resp. rate + lung tissue more impermeable + infiltration of protein and fibrin rich fluids + hyaline membrane formation → impairment of gas exchange → hypoxemia → central cyanosis + pulmonary hypertension |
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Drugs commonly used for asthma ?
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short acting beta2 adrenergic agonists
Quick relief, administer by inhalation. Later, give corticosteroids for daily use. |
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Pathophysiology of asthma
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Type I hypersensitivity reaction
Allergen → Acute response (early phase) 10-20 min: attract IgE coated mast cells → release histamine, leukotrienes, interleukins, and prostaglandins → infiltrations of inflammatory cells, brochospasm, mucosal edema by increased permeability, increased mucus secretions Late phase response (4 – 8 hrs) Airway inflammation → edema, impaired mucociliary function, epithelial injury |
