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NURS 406 : PATHO : TEST QUESTIONS WITH COMPLETE
SOLUTIONS
what is the primary mechanism that causes GERD -- Answer โโ lower esophageal sphincter (LES) dysfunction GERD -- Answer โโ Reflux of gastric contents into the esophagus 2 types of GERD -- Answer โโ 1. physiologic (damage but no symptoms)
- nonerosive (symptoms but minimal damage) 3 things that can cause LES dysfunction -- Answer โโ 1. drugs that relax LES
- hiatal hernia
- increased abdominal pressure 6 manifestations of GERD -- Answer โโ 1. Heartburn
- asthma trigger
- chronic cough
- sinusitis
- laryngitis
- Upper abdominal pain
4 complications of GERD -- Answer โโ 1. mucosal injury and inflammation
- fibrosis
- cancer
- Barret esophagus dysplastic changes and possible remodeling of the esophagus -- Answer โโ Barret esophagus 4 medications used to treat GERD -- Answer โโ 1. proton pump inhibitors
- H2 receptor antagonist
- prokinetics
- antacids what cells are replaced in esophagus with GERD? -- Answer โโ columnar cells replace squamous epithelium autonomic constriction and relaxation of muscles creating wave-like movements. -- Answer โโ Peristalsis what three things regulate peristalsis -- Answer โโ 1. Enteric Nervous System
- Vagal Nerve
- Hormones breakdown of ingested food into smaller parts -- Answer โโ Digestion movement of nutrients from GI tract into body -- Answer โโ Absorption breaking & making of usable energy from digested food -- Answer โโ Metabolism
- sedentary
- low-residue diet
- low fluid
- holding it issues with intestinal motility reduces number and amount of stools -- Answer โโ slow transit constipation pelvic floor muscles, anal sphincter fail to relax -- Answer โโ pelvic floor/outlet dysfunction constipation what are 3 examples of secondary constipation -- Answer โโ 1. opioid-induced constipation
- pregnancy
- spinal cord injury 4 complications of constipation -- Answer โโ 1. fecal impaction
- compression of capillaries can cause ischemia/necrosis
- engorgement of hemorrhoidal veins/thrombosis
- anal fissures presence of loose, watery BMs -- Answer โโ Diarrhea 4 mechanisms of diarrhea -- Answer โโ 1. osmotic
- secretory
- motility
- inflammatory
Non-absorbable substance draws water into the GI tract -- Answer โโ osmotic diarrhea over-secretion of mucus or inhibition of sodium absorption (micro-organisms) -- Answer โโ Secretory diarrhea what do you typically associate secretory diarrhea with? -- Answer โโ infection (C. diff) faster transit time by physiological change in intestine, neurological change or medication -- Answer โโ Motility diarrhea 3 complications of diarrhea -- Answer โโ 1. dehydration
- electrolyte imbalance
- metabolic acidosis 3 ways to evaluate diarrhea -- Answer โโ 1. stool culture
- endoscopy
- biopsy 3 types of stimulus that cause abdominal pain -- Answer โโ 1. mechanical
- inflammatory chemicals
- ischemic pain what is a mechanical stimulus for abdominal pain -- Answer โโ stretching and distention from edema, congestion what is an inflammatory stimulus for abdominal pain -- Answer โโ bradykinin, histamine, serotonin etc. stimulating nerve endings
suspensory muscle that supports the fold of the gut between the duodenum and jejunum -- Answer โโ Ligament of Trietz 6 causes of an upper GI bleed (esophagus, stomach, duodenum) -- Answer โโ 1. Ulcerations
- Varices
- Tears
- Cancer
- Drugs
- Inflammatory Diseases 4 causes of lower GI bleed (jejunum, ileum, colon, rectum) -- Answer โโ 1. polyps
- inflammation
- Cancer
- Hemorrhoids lab marker used to see if we are digesting blood proteins (to see if you have an upper or lower GI bleed) -- Answer โโ BUN lab that measures hepatocellular and myocyte injury -- Answer โโ AST (aspartate sminotransferase) lab that measures hepatocellular injury -- Answer โโ ALT (alanine transaminase) is AST or ALT more specific? -- Answer โโ ALT lab that measures hepatobiliary disease or bone breakdown -- Answer โโ Alkaline phosphatase
lab that measures breakdown of RBC -- Answer โโ bilirubin lab that is elevated in hepatobiliary disease (not bone breakdown) -- Answer โโ GGT (gamma-glutamyl transferase) Protein that maintains osmotic/oncotic pressure in the blood and is produced by the liver (measures liver function) -- Answer โโ Serum albumin clotting cascade factors produced by the liver - measures liver function -- Answer โโ INR, PT (prothrombin time) lab that measures pancreatic function - breaking down carbs -- Answer โโ Amylase lab that measures pancreatic function - breaking down fats -- Answer โโ Lipase lab that measures the presence of antibodies -- Answer โโ Serology 2 types of angiography for a GI bleed -- Answer โโ 1. percutaneous transhepatic cholangiography (PTC)
- endoscopic retrograde cholangiopancreatography (ERCP) inflammatory disorder of gastric mucosa -- Answer โโ Gastritis mechanism of action for how NSAIDs cause gastritis -- Answer โโ NSAIDS inhibit COX 1 by inhibiting prostaglandin synthesis (stimulates mucous and suppresses inflammation), cause hypermotility (mucosal compression/injury) 4 treatments for gastritis -- Answer โโ 1. H2 receptor antagonist
- PPI
pain timing for duodenal and gastric ulcers -- Answer โโ duodenal ulcer: 30min - 2 hours after eating (empty stomach) or intermittent, t night gastric ulcer: immediately after eating describe the pain pattern between duodenal and gastric ulcers -- Answer โโ duodenal ulcer: pain - food/antiacid - relief gastric ulcer: food - pain/ pain - antiacid-relief describe pain and symptom frequency with duodenal and gastric ulcers -- Answer โโ duodenal ulcer: acute (remission - exacerbation) gastric ulcer: chronic, more severe 3 types of malabsorption syndromes -- Answer โโ 1. pancreatic exocrine insufficiency
- lactase deficiency
- bile salt deficiency (fats) syndromes where there is interference of nutrient absorption in the small intestine -- Answer โโ malabsorption syndromes 2 mechanisms of action for malabsorption syndromes -- Answer โโ 1. enzyme deficiency
- inadequate secretion or absorption inflammatory bowel disease pathophysiology (9 steps) -- Answer โโ 1. alterations in mucosal barrier
- changes in immunity/microorganisms
- activation of dendritic cells and transport to mesenteric lymph nodes
- differentiation of naive T cells to Th1, Th2, Th17 or Treg
- proinflammatory cytokines and chemokines damage intestinal epithelium
- fluid leaks into GI
- mucosa bleeds, erosions become ulcers
- mucosa may swell, thicken, become necrotic
- loss of mucosal absorptive function 6 risk factors for inflammatory bowel diseases -- Answer โโ 1. autoimmune dysfunction
- age
- genetics
- infections
- geographical location
- inappropriate diet 4 red flags for inflammatory bowel diseases -- Answer โโ 1. peripheral arthritis
- oral apthous ulcer
- episcleritis
- erythema nodosum common complication with inflammatory bowel disease -- Answer โโ anemia how do you know the location of inflammation with inflammatory bowel disease? -- Answer โโ barium enema 4 labs you'll see with inflammatory bowel disease -- Answer โโ 1. Increased WBC
- increased ESR
- increased CRP
3 medications used to treat inflammatory bowel disease -- Answer โโ 1. corticosteroids
- immunosuppressants/immunomodulators (anti-TNF)
- anti-inflammatories outpouching/hernias of mucosa through the colon's smooth muscle layer -- Answer โโ diverticula 2 complications of diverticular disease -- Answer โโ 1. rupture of diverticula
- peritonitis 3 accessory organs of digestion -- Answer โโ 1. liver
- gallbladder
- pancreas 5 complications of liver disorders -- Answer โโ 1. portal hypertension
- ascites
- hepatic encephalopathy
- jaundice
- hepatorenal syndrome elevated blood pressure in the portal venous system (>5mmHg) -- Answer โโ portal hypertension what causes portal hypertension -- Answer โโ obstruction of blood flow through portal system (Cirrhosis) 2 complications of portal hypertension -- Answer โโ 1. esophageal varices
- splenomegaly
treatment of portal hypertension -- Answer โโ no definitive treatment accumulation of fluid in the peritoneal cavity -- Answer โโ ascites 3 treatments for ascites -- Answer โโ 1. sodium restriction
- diuretics
- possible paracentesis main mediator of hepatic encephalopathy -- Answer โโ ammonia which cannot be metabolized by a malfunctioning liver 2 treatments for hepatic encephalopathy -- Answer โโ 1. lactulose
- rifaximin renal failure related to liver dysfunction -- Answer โโ hepatorenal syndrome type of hepatorenal syndrome related to massive GI or esophageal bleeding and resulting hypotension -- Answer โโ Type 1 type of hepatorenal syndrome related to increase in vasoactive substances due to failure of the liver to metabolize them -- Answer โโ Type 2 compare onset between type 1 and type 2 hepatorenal syndrome -- Answer โโ type 1: acute type 2: slower onset 2 liver disorders -- Answer โโ 1. hepatitis
4. N&V
what is occurring during the icteric phase of hepatitis -- Answer โโ jaundice and inflamed liver where do you have pain with a damaged liver -- Answer โโ RUQ 5 extrahepatic symptoms for hepatitis -- Answer โโ 1. vasculitis
- pain in synovial joints
- pericarditis or myocarditis
- glomerulonephritis
- platelets, RBCs, granulocytes what is occurring during the chronic phase of hepatitis -- Answer โโ cells try to regenerate which can lead do dysplasia (cancer) or cirrhosis transmission of Hepatitis A -- Answer โโ fecal-oral, blood (contaminated food/water, needles) transmission of Hepatitis B -- Answer โโ blood & body fluids (sexual contact, needle sharing, birth) transmission of Hepatitis C -- Answer โโ blood which type of Hepatitis does not have a vaccine -- Answer โโ Hepatitis C trajectory of hepatitis A -- Answer โโ self-limited
trajectory of hepatitis B -- Answer โโ may be acute or chronic (cirrhosis, cancer, and death) what is the only time in which you can get hepatitis D -- Answer โโ if you have hepatitis B trajectory of hepatitis C -- Answer โโ may be acute or chronic (cirrhosis, cancer, and death) treatment of hepatitis A -- Answer โโ supportive care treatment of hepatitis B -- Answer โโ antiviral treatment; immunoglobulin treatment treatment of hepatitis C -- Answer โโ direct acting antivirals (DAAs) what does HBsAg show? -- Answer โโ if they have an active (acute or chronic) infection what does Anti-HBs show? -- Answer โโ if they have been vaccinated or a past infection what does Anti-HBc show? -- Answer โโ past or current infection irreversible inflammatory fibrotic liver disease -- Answer โโ cirrhosis which type of hepatitis is most likely to cause cirrhosis? -- Answer โโ hepatitis C what is the key pathophysiology of liver cirrhosis -- Answer โโ liver attempting regeneration is interrupted by hypoxia, necrosis, atrophy and liver failure
- surgical debridement
- NG suction 3 phases of bone injury/healing -- Answer โโ 1. initial inflammatory phase
- repair phase
- remodeling phase 3 steps for the initial inflammatory phase of bone injury/healing -- Answer โโ 1. hematoma formation between fractured bone edges
- bone tissue at edge of fracture dies
- osteoblasts and osteoclasts activated and produce subperiosteal procallus along outer surface over broken aspect of bone 3 steps for the repair phase of bone injury/healing -- Answer โโ 1. capillary development, mononuclear cells and fibroblasts begins transforming hematoma into granulation tissue
- osteoblasts synthesize collagen and matrix, which mineralize to become callus
- clinical union of fracture, ossification what happens during the remodeling phase of bone injury/healing -- Answer โโ unneeded callus is resorbed and trabeculae form along lines of stress breakdown of muscle cells and release of their contents -- Answer โโ rhabdomyolysis bone breakdown is faster than bone formation -- Answer โโ osteoporosis cell that maintains bone tissue -- Answer โโ osteocyte cells that forms bone matrix -- Answer โโ osteoblast
cell that resorbs bone -- Answer โโ osteoclast 4 disease characteristics of osteoporosis -- Answer โโ 1. low bone mineral density (BMD)
- impaired bone structural integrity
- decreased bone strength
- risk of fracture 3 possible pathways for the OPG/RANKL/RANK system -- Answer โโ 1. Osteoblasts synthesize and secrete RANKL which binds RANK allowing their activation, maturation and prolonging the survival of osteoclasts
- osteoblasts also secrete OPG, a soluble RANKL decoy receptor, which prevents RANKL binding to RANK, inhibiting osteoclastogenesis
- RANKL can also bind the LGR4 receptor on the surface of osteoblasts, triggering signals of mineralization and bone formation what is the main pathophysiology in osteoporosis -- Answer โโ alteration in the RANKL/RANK/OPG system how does estrogen impact osteoporosis -- Answer โโ stimulates OPG secretion and downregulates RANKL lower estrogen means increased RANKL expression (which is on the osteoclasts) 3 risk factors of osteoporosis -- Answer โโ 1. genetics
- menopause
- medications (corticosteroids)
