MEDS5009 CASE STUDY EXAM Flashcards by Taylor Cumming

small pouch-like bulge or pocket that can appear anywhere along GIT

symptoms: pain and tenderness in lower left quadrant, nausea and vomiting, fever, elevated WBC count, diarrhoea, flatulence, bloating, abdominal pain, cramps, weight loss, weakness

Diverticulum

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Occurs as a result of backward flow of gastric contents into oesophagus

caused: increase in gastric volume and intra-abdominal pressure, lowered tone of oesophageal sphincter

symptoms: dyspepsia, regurgitation, hypersalivation, dysphagia, chronic cough, asthma, chest pain, flatulence, bloating, nausea, vomiting

Gastroesophageal reflux disease (GERD)

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inflammation of stomach and stomach lining characterised by absence of grossly visible erosions and presence of chronic inflammatory changes, and eventually atrophy of glandular epithelium of stomach

causes: NSAIDS, H.pylori, alcohol
symptoms: vomiting, pain, nausea
complication: ulcer formation

Gastritis

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sore that develops in lining of stomach and duodenum

causes: NSAIDS, H.pylori infection
symptoms: abdominal pain (at night, relieved by antacids, occur 2-3 hours after meal), nausea, indigestion, vomiting blood, blood in stool// black stool, weight loss, fatigue
complications: hemorrhage, obstruction, perforation

Peptic Ulcer

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recurrent, granulomatous type of inflammatory response that can affect any area along GIT (mainly ileum, colon), characterised by skip lesions

symptoms: diarrhoea, fistulas, strictures, perianal abscesses complications: malabsorption

Crohn’s Disease

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non-specific continuous inflammatory condition of colon

symptoms: diarrhoea, rectal bleeding
complications: development of cancer

ulcerative colitis

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normal CRP

< 10 mg/L

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decrease in bile flow through canaliculi and reduction in secretion of water, bilirubin, bile acids from hepatocytes
complications: fatty changes, destruction of CT, accumulation of bile products and debris, fibrosis, biliary cirrhosis

cholestasis

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yellow discolouration of skin and deep tissues as result of high levels of bilirubin in blood, due to imbalance between production and excretion

jaundice

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RBC destruction in excess of capacity of liver

elevated unconjugated bilirubin, normal stool colour

pre-jaundice

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impaired capacity of liver to remove bilirubin from blood and conjugate it

elevated conjugated and unconjugated bilirubin, dark urine, elevated serum alkaline phosphatase

intra-jaundice

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bile flow obstructed at any point between hepatic duct and intestine

elevated conjugated bilirubin, grey stool, dark urine, elevated serum alkaline phosphatase

post-jaundice

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single stranded RNA virus transmitted through fecal oral route (contaminated food and water)

symptoms: fever, nausea, malaise, abdominal discomfort, dark urine, jaundice

last 2 months, no carrier or chronic status, vaccine

hepatitis A

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double stranded DNA virus transmitted through blood or serum (sexual or oral contact)

carrier status and chronic, vaccine

hepatitis B

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single strand RNA virus which is the most common cause of chronic hepatitis, cirrhosis and cancer

transmitted by high risk drug use and sexual behaviour

no vaccine

complications: fibrosis leading to cirrhosis, end-stage liver disease, hepatocellular cancer

hepatitis C

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chronic inflammatory reaction of liver lasting more than 3 months characterised by elevated liver enzymes

symptoms: fatigue, malaise, loss fo appetite, jaundice

chronic viral hepatitis

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surpass the capacity of the liver to metabolise alcohol, resulting in the by-products of alcohol metabolism contributing to liver damage

stages: simple steatosis, alcoholic hepatitis, cirrhosis

alcohol liver disease

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metabolic dysfunction affecting liver, lipid accumulation within hepatocytes and formation of free radicals

stages: simple steatosis (over-nutrition), non-alcoholic hepatitis, cirrhosis

non-alcoholic fatty liver disease

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normal ALT

<35 U/L, test for hepatocellular injury

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normal AST

<40 U/L, test for hepatocellular injury

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GGT

alcohol abuse identification

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serum albumin and prothrombin time

reflect liver synthetic capacity

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ALP and GGT

cholestatic bile flow markers

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normal serum albumin

3.5 - 5.5 g/dL

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end-stage chronic liver disease, most functional tissue replaced with fibrous tissue symptoms: weight loss, weakness, anorexia, diarrhoea, jaundice, abdominal pain

cirrhosis

increased resistance to flow into portal venous system and sustained portal vein pressure complications: ascites, splenomegaly, portosystemic shunts

portal hypertension

sudden and massive liver destruction or progressive damage to the liver resulting in loss of 80-90% functional capacity of the liver

liver failure

build up of fatty deposits in arteries characterised by development of atheromatous lesions within intimal lining of arteries that protrude and eventually obstruct flow development: endothelial cell injury, migration of inflammatory cells, smooth muscle cell proliferation and lipid deposition, gradual development of plaque with lipid core complications: thrombosis, ischemia, obstruction, aneurysm, myocardial infarction, CHD

atherosclerosis

heart disease caused by impaired coronary blood flow causes: genetics, age, sex, smoking, high BP, high cholesterol, excessive alcohol, stress, inactivity, family history, obesity, diabetes, thrombosis

coronary heart disease

coronary heart disease where no evidence of serum markers for myocardial damage symptoms: unexpected chest pain, unaltered by rest and nitroglycerin, unrelenting, unsurvivable without treatment

unstable angina

coronary heart disease with serum markers of myocardial damage

NSTEMI

coronary heart disease (heart attack) characterised by ischemic death of myocardial tissue associated with atherosclerotic disease of coronary arteries complications: death, arrhythmia, rupture, heart failure, valve disease, disorders of cardiac conduction,

STEMI

dysfunction of heart valves causing disturbances in blood flow, produce blood flow turbulence stenotic - decrease in blood flow through valve, resulting in impaired emptying and increased work demands regurgitant - permits blood flow to continue when valve closed

valvular heart defects

complex syndrome from any functional or structural disorder of heart that increases risk of low CO and systemic/pulmonary congestion cause: anything that reduces pumping ability of heart

heart failure

congestion of peripheral tissues symptoms: swelling, weight gain, edema, lethargy, large neck veins, irregular HR, nausea, increased girth abdomen

right heart failure

decreased CO and pulmonary congestion symptoms: difficulty breathing, rales, orthopnea, weakness, nocturnal paroxysmal dyspnea, increased HR, nagging cough, gaining weight

left heart failure

known heart failure but no limitations during activity

class 1 heart failure

heart failure and only slight limitations during activity (not extreme fatigue, palpitations or angina)

class 2 heart failure

heart disease, comfortable at rest but ordinary activity results in chest pain, fatigue, palpitations

class 3 heart failure

marked progressive heart disease, not comfortable at rest

class 4 heart failure

sustained elevated BP within arterial circuit causes: poor diet, dyslipidaemia, tobacco, alcohol, fitness, obesity complications: angina, myocardial infarction, heart failure, stroke, CKD

hypertension

<120 SBP and <80 DBP

normal BP

120-129 SBP and <80 DBP

elevated BP

130-139 SBP or 80-89 DBP

stage 1 hypertension

>140 SBP or >= 90 DBP

stage 2 hypertension

lipid levels too high, characterised by high LDL, high TAG, low HDL and high total cholesterol causes: genetic, sedentary lifestyle, excessive dietary intake, aging, certain drugs

dyslipidaemia

total cholesterol >= 5.5 mmol/L LDL >= 3.5 mmol/L HDL <1.0 mmol/L (men), <1.3 mmol/L (women) TAG >= 2.0 mmol/L

lipid profile dyslipidaemia

<2.5 mmol/L

normal LDL

>1.0 mmol/L

normal HDL

<1.7 mmol/L

normal TAG

chronic, systemic illness characterised by alterations in function of tissues and organs due to excess adiposity (enlarged body fat stores) causes: poor diet, low PA, high BMI, imbalance between intake and expenditure, genetic pre-disposition complications: insulin resistance, increased risk T2DM, increase risk of cancer

obesity

<18.5 kg/m2

underweight BMI

18.5 - 24.9 kg/m2

normal BMI

25 - 29.9 kg/m2

overweight BMI

>30 kg/m2

obese BMI

>102 cm (men), >88 cm (women)

obese waist circumference

accumulation of visceral fat endocrine organ secretes inflammatory mediators, adipokines, FFA

insulin resistance pathogenesis

insulin deficiency due to viral damage to beta cells, sudden onset and requires insulin treatment

type 1 diabetes

disease of insulin resistance and beta cell dysfunction causes: genotype, family history, poor diet, lack of physical exercise, aged 40-75, obese, asian or african origin complications: hyperosmolar hyperglycemic state, microangiopathy, gangrene, DKA

type 2 diabetes

>= 7.0 mmol/L

hyperglycemia fasting blood glucose

>= 11.1 mmol/L

hyperglycemia random blood glucose (PP)

>= 6.5%

hyperglycemia HbA1c

uncontrolled division of cells which crowd out normal cells, function abnormally and destroy functioning of major organs causes: smoking, obesity, physical activity, poor nutrition, alcohol, carcinogens

cancer

1. initiation (DNA damaged) 2. promotion (modified growth, mutations, promote oncogenes, inactivate tumour suppressor genes) 3. transformation (mutations) 4. progression

carcinogenesis

ongoing decrease in skeletal muscle mass with or without fat loss resulting in progressive functional impairment, weakens chemo and increased mortality

cancer cachexia

metabolic bone disease characterised by loss of mineralised bone mass causing increased adiposity of skeletal and increase risk of fractures imbalance bone formation and resorption

osteoporosis

progressive and generalised skeletal muscle disorder that involves accelerated decrease muscle mass and function causes: anything decreases muscle mass, low protein and energy, micronutrient deficiencies, malabsorption, GI conditions, other diseases, reduced physical activity consequences: increase risk of falls and fractures

sarcopenia

decrease muscle mass + low BMD, which increases risk of falls and fractures causes: ageing, smoking, chronic disease, reduces physical activity, poor diet, vitamin d deficiency

osteosarcopenia

softening of bones due to under mineralisation in remodelling process

osteomalacia

localised excessive bone turnover and disorganised formation of new bone tissue rapid bone resorption followed by chaotic bone deposition with low quality bone

Paget's disease

systemic inflammatory disorder leading to development of joint and synovial inflammation via autoimmune mechanism

rheumatoid arthritis

slow progressive destruction of articular cartilage of weight bearing joints and fingers causes: inflammation caused by cartilage trying to repair itself

osteoarthritis

group of disorders characterised by increased serum uric acid and urate crystal deposits in kidney and joints

gout

combination of obesity with low skeletal muscle mass and function

sarcopenic obesity

acquired, persistent impairement of mental abilities, accompanied by changes in personality and behaviour, not a normal part of ageing cause: disease, head trauma, death to neurons (unknown cause)

dementia

progressive, degenerative disorder that attacks neurons resulting in memory, thinking and language loss and behavioural changes causes: linked to amyloid plaques, high fat diet and leaky blood brain barrier

Alzheimer's disease

immune-mediated disorder where body's autoimmune system attacks myelin sheath of neuronal axons progression: relapsing-remitting, secondary progressive, primary progressive, progressive relapsing

multiple sclerosis

widespread reduction of blood flow to brain causes: low perfusion, decrease blood flow, chronic hypoxia, hypoglycaemia

global cerebral ischemia

regional ischemia which results in focal neurologic deficits lasting more than 24 hours includes thrombotic, embolic and lacunar strokes

ischemic stroke

MEDS5009 CASE STUDY EXAM Flashcards

(79 cards)