Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
59 Cards in this Set
- Front
- Back
|
What two factors is the progression of ESRD based on (biochemical labs)? |
reduction in GFR and creatinine clearance. |
|
|
What GFR is clinical ESRD? |
<15mL/min |
|
|
List 4 causes of CKD |
HTN, diabetes, glomerulnephritis, UTI. |
|
|
What is one of the first signs of renal failure (biochemical?) |
hyperfiltration leading to proteinuria. |
|
|
How is RAAS involved in progression of renal failure? |
RAAS activation causes inflammation and fibrosis of the glomerulus and tubules. |
|
|
What occurs in bronchitis? |
Inflammation of the bronchial tubes (caused by smoking, etc.) as well as blockage from excessive mucus production; edema, hyperplasia, frequent respiratory infections (mucus). |
|
|
What are some signs of COPD? |
obesity, malnutrition/weight loss/cachexia, clubbing of the finger nails, barrel chest, cyanosis. |
|
|
What occurs in emphysema? |
Destruction of the alveoli tissue; decreases air flow (air trapping) due to loss of surface area and decreased amounts of surfactant. |
|
|
What are some symptoms of COPD? |
dysphagia, dyspnea, excess mucus, chronic mouth breathing, taste alterations, depression |
|
|
What are some additional complications involved in the patho of COPD? |
Pulmonary HTN, respiratory infections, weight loss/malnutrition/systemic inflammation, osteoporosis, depression, CAD, lung cancer, GERD. |
|
|
What are some etiologies of Heart Failure? |
age, RAAS (HTN), diabetes, CAD, Obesity, Sedentary Lifestyle, Nutrient deficiency (thiamine), Western diet |
|
|
How does the heart try to compensate for CHF? (3 methods) |
1. heart enlargement 2. increase blood volume (RAAS) 3. Increase sympathetic activity (increase HR, peripheral resistance) |
|
|
What is systolic HF? |
The heart is unable to pump normally leading to inadequate blood supply to body and lungs |
|
|
What is diastolic HF? |
The heart is unable to fill efficiently during relaxation (diastole), resulting in less blood pumped out. |
|
|
What is RHF? |
Unable to pump blood to the lungs via the pulmonary arteries. |
|
|
What is LHF? |
Unable to pump blood to the body via the aorta. |
|
|
What are the forward/backward effects of RHF? |
Forward: pulmonary HTN Backward: Peripheral edema |
|
|
What are the forward/backward effects of LHF? |
Forward: inadequate blood flow to cells of the body (fatigue, impaired growth/function, weakness, SOB, etc.) Backward: pulmonary congestion |
|
|
________HF causes__________HF due to weakening of the muscle over time. |
Left HF, Right HF |
|
|
What are some symptoms attributed to HF? |
SOB/dyspnea, dry, hackig cough, abnormal breath sounds, confusion/impaired thinking, fatigue, anorexia. |
|
|
What are some signs of HF? |
edema (peripheral, ascites, pulmonary, pleural effusion), weight gain, increased HR, cyanotic/pale skin, cachexia |
|
|
What are some initial signs of undiagnosed diabetes? |
polyphagia, polydipsia, polyuria, ketosis, fatigue |
|
|
What characterizes Type 2 diabetes? |
peripheral insulin resistance, defective insulin secretion, increased GNG, altered gut microbiome. |
|
|
What causes/influences insulin resistance? |
inflammation which is typically caused by obesity (accumulation of pro-inflammatory cytokines and immune factors which impair signaling in local cell surrounded by adipose tissue). Also hormones like leptin. |
|
|
List the basic steps in the development of an atherosclerotic plaque (8 steps) |
1. irritant (LDL, smoke, chronic high BP) 2. endothelial dysfunction (inflammation, immune activation) 3. LDL invades vessel wall (attractsmonocytes/macrophages) 4. Foam cells/fatty streak (macrophages engulf LDL, oxidation produces foam cells) 5. migration to tunica intima 6. formation of fibrous cap 7. calcium deposition 8. Rupture of cap (can result in embolism-pulmonary or cerebral) |
|
|
T or F: CVD is a disease of impaired cholesterol storage. |
False it is a complex interaction of risk factors which leads to an inflammatory process in the arterial wall. |
|
|
T or F: The plaque in the lumen is considered a late-stage manifestation of atherosclerosis. |
True, by the time the plaque is visible it has already been growing in the intima for quite some time. |
|
|
What is the cellular basis of obesity? |
Adipocyte |
|
|
T or F: the adipocyte is metabolically active endocrine gland? |
True, it produced several peptide and metabolites that are involved in controlling body weight, appetite, and inflammation. |
|
|
What occurs with the presence of large amounts of adipocytes? |
secretion of inflammatory cytokines and decreased adiponectin, insulin resistance, abnormal appetite regulation |
|
|
What two main hormones are secreted from adipose tissue and what is their role? |
Adiponective and leptin 1. Adiponectin is involved in inflammation and low levels are seen in those with obesity. 2. Leptin is a "satiety" hormones" made my adipose cells that helps to regulate energy balance by inhibiting hunger. Leptin resistance is seen in obesity. |
|
|
What are the 5 characteristic of metabolic syndrome according to Grundy, et.al.? |
1. Abdominal obesity (>40" men, >35" women) 2. Triglycerides >=150mg/dL 3. BG >= 110mg.dL fasting 4. HDL: <40mg/dL men,<50mg/dL women 5. BP >=130/85 |
|
|
What is said to be the main driver of the metabolic syndrome? |
insulin resistance |
|
|
How is dyslipidemia involved in the pathogenesis of the metabolic syndrome? |
1. increased triglycerides in the LDL 2. Decreased Apolipoprotein A and HDL concentrations. 3. increase in plasma FFAs due to insulin resistance-->increased lipolysis |
|
|
How is BP involved in the patho of MetS? |
insulin resistance leads to abnormal vascular reactivity and causes vasoconstriction |
|
|
Elevated plasma glucose? |
overall insulin resistance/diabetes. |
|
|
Abdominal obesity? |
increase the risk for IR |
|
|
What are three things that promote a pro-inflammatory state in MetS? |
1. increased FFA concentrations/oxidative stress 2. obesity 3. insulin resistance |
|
|
Metabolic Syndrome has also been referred to as____________-______________ |
pre-diabetes |
|
|
What does Dandona recommend for treating metabolic syndrome? Why? |
Caloric restriction-Dandona subscribes to the mismatch hypothesis which postulates that our metabolism is 'mismatched' to the overnutrition/calories in the westernized diet. Caloric restriction is said to improve insulin response and decrease inflammation/oxidative stress. |
|
|
What diseases does MetS increase risk for? |
diabetes, CVD, CHF, ASCVD events (stroke, MI), atherosclerosis. |
|
|
According to Grundy, what are some long-term and short-term risks associated with MetS? |
long-term: T2DM, ASCVD/ASCVD events short term: CAD |
|
|
What is primary HTN? |
HTN that is caused by an indirect etiology such as smoking, obesity, hyperlipidemia and diabetes. |
|
|
What is secondary HTN? |
something direct such as CKD (increases stroke volume), narrowing of the aorta, etc. |
|
|
T or F: HTN is usually asymptomatic or has non-specific symptoms |
true |
|
|
What are some long-term effects of HTN? |
hemmorhage of arteries from constant pressure, arteriosclerosis (hardening of the arteries), retinopathy, nephropathy, left cardiomegaly/MI, HF. |
|
|
At what level is HTN classified? |
Stage 1: systolic 140-159, diastolic 90-99 Stage 2: >160, >100 Pre-HTN: 120-139, 80-89 |
|
|
How does IR lead to HTN? |
Obesity-->increased insulin resistance-->insulin increases and stimulates SNS-->activate RAAS-->increased reabsorption of Na-->high BP. |
|
|
What two components "set points" are involved in BP? |
Cardiac output=SV+ HR |
|
|
What causes increased heart rate? |
increased SNS, decreased PSNS |
|
|
What causes increased CO? |
increased SV: larger heart, epinephrine, norepinephrine |
|
|
What causes increased peripheral resistance? |
stress increase vasconstriction, RAAS activation (tensinogen), endothelial dysfunction (imbalance between vasodilators/contrictors in favor of constrictors. |
|
|
What is it called when HTN leads to vessel bursting? |
aneurysm |
|
|
What are the diagnostic criteria for prediabetes? |
A1C 5.7-6.4% Fasting: 100-125mg/dL |
|
|
Diagnostic criteria for diabetes |
OGTT: >=200mg/dL random: >=126mgl/dL A1C >=6.5% |
|
|
glycemic targets for healthy adults with diabetes? |
A1C: <7% fasting glucose: 100-130mg/dl |
|
|
glycemic targets for non-critically ill adults with diabetes? |
preprandial: <=140mg/dL postprandial: <=180mg/dL |
|
|
glycemic targets for critically ill adults with diabetes? |
preprandial: <180mg/dL postprandial: 140-180mg/dL |
|
|
glycemic targets for elderly adults with diabetes? |
A1C: Healthy: <7.5% Intermediate: <8.0% Complex <8.5% PPG: 90-130 90-150 100-180 Peak Post Prandial: 90-150 100-180 110-200 |
