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GNRS 610: Test #3 Study Guide Unit-6 Epidemiology
- Levels of disease prevention Primary Prevention The process of altering susceptibility or reducing exposure. Its interventions are carried out during the stage of susceptibility. e.g. vaccination and immunization > Patient does not have any disease at this time. Goal is to reduce the risk of disease. Secondary Prevention The early detection and prompt treatment of a disease at the earliest possible stage. Its measures are carried out during the preclinical stage. Screening programs are designed to detect specific diseases in their early stages e.g. Pap smear and mammography > Patient has the disease, but it is early on in the process and usually asymptomatic. Screening allows us to catch the presence of the disease early on. Tertiary Prevention Its measures are implemented during the middle or late stages of clinical disease to alleviate disability and restore effective functioning. > Reduce morbidity and mortality in a diseased person. Primordial Prevention: Includes policies that promote general health in a community (e.g. no smoking signs, warning labels on cigarette packs, taking lead out of gasoline) - Incidence vs prevalence
https://www.omnicalculator.com/health/ incidence-rate
- Prevalence = Incidence rate x Average duration of disease *Only applicable when prevalence is LOW (< 10%) Short duration diseases (e.g., common cold): Prevalence = Incidence Chronic diseases due to large number of existing cases (e.g., diabetes): Prevalence > Incidence https://www.mdapp.co/prevalence-rate-formula- calculator-586/ https://www.mdapp.co/incidence-rate-calculator-579/ - Calculating the number needed to treat (NNT) Number needed to treat (NNT): # patients needed to be treated to achieve one favorable outcome #1. Calculate ARR Absolute risk reduction (ARR) = Experimental event rate (EER) – Control event rate (CER) #2. Use ARR to calculate NNT Number needed to treat (NNT) = 1/𝐴𝑅𝑅 https://www.omnicalculator.com/health/nnt - The 2x2 table; definitions of, and calculating sensitivity, specificity, PPV, and NPV TP: True positive (Test is positive and disease is present). FP: False positive (Test is positive but disease is not present). FN: False negative (Test is negative but disease is present). TN: True negative (Test is negative and disease is not present).
- How to calculate sensitivity? a. Start w/ TP and go down to FN b. True positive / True positive + False negative
- How to calculate specificity?
a. A highly specific test is good for RULING IN the disease when it is positive (SpIN) b. A specific test should be done after a sensitive test has been positive, and that is to confirm the diagnosis c. Specificity is not related to the prevalence of the disease d. If specificity increases, PPV increases e. When specificity decreases, the test’s utility as a diagnostic test is diminished because the test fails to identify those not having the disease (too many false positives)
- Reliability, precision, and accuracy What is the term for when you repeat a test multiple times and the result is always the same? RELIABILITY Reliability means reproducibility of the results and does not necessarily mean that these results are correct. What is the term for when you repeat a test multiple times and there is a very narrow range of results (clustering)? PRECISION Precision does not necessarily mean that the results are correct. What is the term for when the results are reliable and truly diagnose a condition (correct)? ACCURACY Accuracy is the combination of high sensitivity and high specificity. Such tests are used to be called “The Gold Standard” tests - Compare and contrast the different study designs 1. Used to describe the distribution of disease in terms of personal characteristics, geographical distribution, and time. 2. Ask about 4 W’s: Who? What? Where? When? 3. There are 4 types of descriptive studies a. Case reports b. Case series c. Cross-sectional studies d. Correlation 4. Descriptive studies can be considered observational as well. 1. Looks at the origins and causal factors of disease 2. Are usually carried out to test hypotheses formulated from a descriptive study 3. Their goal is to identify factors that increase or decrease disease risk a. Risk is the probability that an event will occur 4. There are 2 types of analytic studies a. Observational i. Cohort studies ii. Case-control studies b. Interventional (also known as experimental studies) i. Randomized controlled trials
- RCTs: The null hypothesis, alpha & beta errors, calculating the power of the study. 1. Null hypothesis a. Interventional studies start with a hypothesis that there will be NO DIFFERENCE between the groups (intervention group & control group) despite the intervention. b. By default, you suppose the null hypothesis is correct until you have enough evidence to reject it c. The alternative hypothesis (Ha or H 1 ) states that there is a difference between groups d. You cannot prove Ha, you can only reject or fail to reject the null hypothesis (H 0 ) 2. Type I error a. Occurs when a null hypothesis is rejected when in fact it is true (incorrectly rejecting a null hypothesis) b. The investigator says that there is a difference between groups when there really isn’t (FP) c. Type I error is also known as alpha error as it is the most common type of error. 3. Type II error a. Failure to reject a null hypothesis when in fact it is false (incorrectly accepting a null hypothesis) b. The investigator says that there is no difference between groups when in fact there is (FN) c. Type II error is also known as beta error https://riskcalc.org/samplesize/ https://www.statology.org/type-ii-error-calculator/ https://www.danielsoper.com/statcalc/calculator.aspx?id= Unit-7 Endocrinology - Water-soluble hormones vs fat-soluble hormones. Water-soluble hormones 1. Mainly proteins (e.g., peptides, polypeptides, Fat-soluble hormones (also referred to as lipid- soluble)
HYPO-thyroidism “Lazy symptoms” HYPER-thyroidism “Crazy symptoms” Primary hypothyroidism: Hashimoto disease Problem is in the thyroid gland itself. In primary, the gland hormone and pituitary hormone are OPPOSITE.
- Low T3/T
- High TSH *being stimulated but not producing Secondary hypothyroidism: Pituitary is compressed by tumor, therefore, TSH is not being released. Problem is outside of the thyroid gland. In secondary, the thyroid gland and pituitary hormone are in the same direction.
- Low T3/T
- Low TSH *not stimulating, so we know this is not a thyroid issue Primary hyperthyroidism: Graves’ disease
- High T3/T
- Low TSH Secondary hyperthyroidism: Pituitary adenoma
- High T3/T
- High TSH First question to ask: Where is the problem? Remember: TSH goes to the thyroid, to stimulate the release of T3 and T
- Case 1 = low thyroid hormones, high stimulating = primary hypothyroidism (being stimulated but not producing)
- Case 2 = low thyroid hormones and low TSH, not stimulating = secondary hypothyroidism
- (thyroid gland responds to TSH so we know its not a thyroid issue)
- Case 3 = normal thyroid hormones and TSH; secondary hypothyroidism, problem with target cells Problem
- Case 2 = pituitary gland prevented from producing TSH, hypofunction of thyroid = secondary hypothyroidism
- Case 2 = adenoma produces hormones, increase in thyroid hormones = primary hyperthyroidism
- Case 3 = destruction to thyroid cells =
primary hypothyroidism
- Hashimoto = Type IV Hypersensitivity Reaction, cell mediated by T-cytotoxic cells which attack the thyroid
- Case 4 = thyroid cell receptors altered, behaves if constantly activated by THS
- Graves disease = Type II Hypersensitivity, antibody mediated, tissue specific antibodies attack specific tissues
- Makes cells hyperfunction = primary hyperthyroidism - Parathyroid disorders: causes & effects on calcium levels Primary Hyperparathyroidism Often caused by a noncancerous growth (adenoma) on one or more of the parathyroid glands, leading to overproduction of parathyroid hormone (PTH). Secondary Hyperparathyroidism Usually a response to low calcium levels in the blood, often due to chronic kidney disease or vitamin D deficiency. Tertiary Hyperparathyroidism Occurs when secondary hyperparathyroidism persists for a long time, causing the glands to become overactive. Effects on Calcium Levels Hyperparathyroidism leads to high levels of calcium in the blood (hypercalcemia) because PTH increases calcium release from bones, reabsorption in kidneys, and absorption from the gut.
- Calcium is responsible for threshold potential (“shelf”). High calcium levels decrease excitability (STABILITY). - Clinical picture: “Kidney stones, Abdominal groans, Bones, and Psychiatric overtones.” Hypoparathyroidism results in low levels of calcium in the blood (hypocalcemia) due to insufficient PTH production.
- Radical thyroidectomy
- If threshold potential is low (low calcium), there will be high excitability
- Patient will have vocal cord spasms > Secure the airway and administer calcium - Hypothalamic/Pituitary axis disorders Hypothalamus stimulates pituitary (except two hormones >> which inhibit anterior pituitary: dopamine and somatostatin) Dopamine inhibits prolactin Thyrotropin releasing hormone (TRH) stimulates TSH and prolactin.
testosterone, so male sex characteristics are present. ANY OTHER CAUSE IS CUSHING SYNDROME. Cushing disease: ACTH-dependent hypercortisolism Cushing syndrome: Clinical manifestations resulting from chronic, excess cortisol. Hyperfunction may be due to ANY other reason. Excessive cortisol from benign tumor secreting cortisol, exogenous cortisol (steroid use), et cetera. Cushing-like syndrome: May develop due to exogenous administration of glucocorticoids
- Disorders of the adrenal cortex: Hypofunction (Primary vs secondary) Primary adrenal insufficiency (Addison disease) 1. Autoimmune destruction of adrenal cortical cells 2. High ACTH 3. High MSH (hyperpigmentation) 4. Low aldosterone a. Low sodium b. Lose water so low BP c. High potassium d. High hydrogen (H+), so metabolic acidosis 5. Low testosterone 6. Low cortisol (low blood sugar, especially in times of stress, stress intolerance) Secondary hypocortisolism (commonly due to suppressed pituitary)
- Lowering of ACTH (for whatever cause)
- Low ACTH
- No hyperpigmentation
- Aldosterone is not affected (because it is not regulated by the pituitary!) a. Sodium, water, potassium, and hydrogen are not affected
- Low cortisol
- Low androgen - Disorders of the adrenal cortex: Effects on sodium and potassium levels. Pituitary controls the pituitary complex ACTH does not affect aldosterone, only cortisol and androgens. Aldosterone is a mineralocorticoid, affects sodium (SAVE SODIUM, PEE POTASSIUM) Hypofunction of adrenal cortex 1. Primary: Autoimmune destruction of the adrenal cortex (all three levels) a. Example: Addison’s disease i. Low aldosterone, cortisol, and androgen levels ii. Clinical picture: Low aldosterone, low sodium, hypovolemia, hypotension; high potassium, acidosis iii. Low cortisol: Low blood sugar, **Hyperfunction of adrenal cortex
- Conditions that increase aldosterone (Hyperaldosteronism)** a. Primary = Problem w/ adrenal cortex i. Adenoma in adrenal cortex 1. Example: Conn’s syndrome b. Secondary = Problem w/ pituitary i. All causes that stimulate RAAS
- Hypotension
difficult to cope with any stress, any stress is a major effort for you! iv. Androgens go down as well.
- May affect sex drive v. When cortisol goes down, and pituitary produces ACTH to stimulate >> ACTH comes w/ MSH (causes pigmentation of the skin, or a tan!)
- Secondary: Pituitary is not making ACTH a. Clinical picture i. Low ACTH does not affect aldosterone (remember!) ii. Cortisol levels will go down iii. Androgen levels will go down iv. Similar to Addison w/o the aldosterone effects (so sodium and potassium will not be affected). v. There will be no skin pigmentation, however. **What happens to sodium and potassium levels in the following conditions?
- Addison’s disease** a. Low aldosterone i. Sodium - - - ii. Potassium +++ 2. Conn’s syndrome a. Hyperaldosteronism (high aldosterone) i. Sodium +++ ii. Potassium - - - 3. Cushing disease/syndrome a. Hypercortisolism (will look like high aldosteronism) i. Sodium +++ ii. Potassium - - -
- Hypovolemia a. CHF b. Renal artery stenosis c. Recall: Aldosterone is a mineralocorticoid i. Affects sodium >> Causes the body to save sodium and pee potassium ii. Clinical picture: High aldosterone levels will result in high sodium and low potassium
- Hypernatremia, which will cause hypervolemia and hypertension)
- Hypokalemia, which will cause alkalosis 2. Conditions that increase cortisol (Hypercortisolism) a. Cortisol is a stress hormone, primarily concerned with blood glucose i. “Glucocorticoid” b. Clinical picture will look like high aldosteronism and excess androgens, as if all three layers of the adrenal cortex have problems i. In women: Acne, amenorrhea, hirsutism c. Clinically known as Cushing disease (high ACTH) or Cushing syndrome (normal ACTH) i. Increased glucocorticoids ii. Increased mineralocorticoids iii. Increased androgens
b. Pain management c. Judicious use of transfusions d. Hydroxyurea (increases synthesis of HbF) e. Genetic counseling and support (preimplantation genetic diagnosis)
- Macrocytic (NORMOCHROMIC) anemias: types, clinical picture, lab diagnosis 1. Pernicious anemia a. Mechanism of anemia i. A lack of intrinsic factor (IF) from gastric parietal cells required for vitamin B absorption ii. Lack of vitamin B12 for erythropoiesis iii. Abnormal DNA & RNA synthesis in the erythroblast iv. Death during maturation b. Primary cause i. Congenital/acquired deficiency of intrinsic factor ii. Genetic disorder of DNA synthesis iii. Gastrectomy or ileal resection iv. Autoimmune chronic atrophic gastritis c. Typical anemia symptoms AND neurologic manifestations i. Nerve demyelination (paresthesias, loss of position and vibratory sense, and spastic ataxia) ii. Loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis) , icterus, splenic enlargement d. Treatment i. Parenteral or high oral doses of vitamin B 2. Vitamin B12 deficiency a. Causes i. Pernicious anemia ii. Gastrectomy, bariatric surgeries, ileal resection iii. Malabsorption (e.g., Crohn’s disease, chronic Metformin therapy) iv. Insufficient intake > Veganism b. Typical anemia symptoms AND neurologic manifestations c. Diagnosis i. High homocysteine, High methylmalonic acid d. Treatment i. Parenteral or high oral doses of vitamin B 3. Folate deficiency anemia a. Mechanism of anemia i. Lack of folate for erythropoiesis ii. Apoptosis of erythroblasts in the late stages of erythropoiesis b. Primary cause i. Dietary folate deficiency (alcoholic, chronic malnourishment) ii. Drugs: Methotrexate, Trimethoprim iii. Pregnancy (associated with neural tube defects) c. Specific symptoms i. Severe cheilosis (scales and fissures of the lips/corners of the mouth)
ii. Stomatitis (ulceration of the buccal mucosa and tongue!) iii. NO neurologic symptoms d. Diagnosis i. High homocysteine, Normal methylmalonic acid e. Treatment i. Oral folate preparations
4. Alcohol-induced anemia a. Mechanism of anemia i. Direct effect causing macrocytosis ii. Indirect effect causing nutritional deficiencies (folate) b. Primary cause i. Severe chronic alcoholism *Additionally referred to as megaloblastic anemias **- Microcytic (HYPOCHROMIC) anemias: types, clinical picture, lab diagnosis
- Iron deficiency anemia** a. Mechanism of anemia i. Lack of iron for hemoglobin production ii. Insufficient hemoglobin b. Primary cause i. Chronic blood loss or dietary iron deficiency **1. Low iron
- Low ferritin
- High TIBC**
- GIT (gastric/colon)
- Menorrhagia
- Pregnancy
- Absorption disorders (e.g., GI surgery) c. Specific symptoms i. Koilonychia (concave, rigid, brittle nails) ii. Glossitis (red, sore, painful tongue) iii. Angular stomatitis (dryness and soreness) iv. Gastritis, neuromuscular alterations, irritability, headache, numbness, tingling, and vasomotor disturbances d. Evaluation i. Low HgB and Hct ii. Low MCV and MCHC iii. Poikilocytosis and anisocytosis (High RDW) iv. Low serum ferritin v. High serum transferrin receptor (sTfR) vi. High total iron-binding capacity (TIBC) vii. 1-2 g/dL higher in HgB after starting iron therapy e. Treatment i. Identify and eliminate source of blood loss ii. Oral ferrous sulfate iii. Newer parenteral sodium ferric gluconate complex in sucrose (Ferrlecit) and iron sucrose injection (Venofer)
b. Primary cause i. Increased fragility of erythrocytes c. Diagnosis i. Regardless of where it occurs, hemolysis is associated with high reticulocytes, high bilirubin, and high LDH
Diabetes
- Kussmaul respirations, acetone breath, CNS depression, and potassium deficiency are all signs of: a. Diabetic kidney disease b. Hyperosmolar hyperglycemic nonketotic syndrome c. Diabetic ketoacidosis d. Diabetic retinopathy
- Mrs. Smith presents to the ER confused, fatigued, pale, and diaphoretic. Her husband states, “She was fine this morning. She did not even skip her medications. She started a new workout program recently and has been working out hard. She actually worked out so hard she lost her appetite and did not eat breakfast.” When reviewing Mrs. Smith’s chart, you noticed a history of DM-I. With this information provided, what would be the diagnosis assumed for Mrs. Smith prior to labs? a. Diabetic nephropathy b. Hyperglycemia c. Hypoglycemia d. Diabetic ketoacidosis
- What is a risk factor for developing type 2 diabetes? a. All choices are correct b. Family history c. Obesity d. Age
- What are the overlapping manifestations of DKA and HHS? a. Dehydration and ketosis b. Hyperglycemia and ketosis c. Hyperglycemia and dehydration d. Hypoglycemia and dehydration
- How to follow up the response of a diabetic patient to treatment? a. Insulin requirements b. Hemoglobin A1C c. Tolerability of physical exercise d. Weight loss
Thyroid disorders
- What is an early sign of “thyroid storm?” a. Tingling sensation on extremities b. Oliguria c. Agitation and confusion d. Facial twisting
- Which is NOT a symptom of myxedema coma? a. Hypoglycemia
b. Hypoventilation c. Hypothermia d. Hypertension
- What is the major cause of primary hypothyroidism in the United States? a. Radiotherapy to the head and neck b. Pituitary tumors c. Hashimoto thyroiditis d. Iodine deficiency
- A person who does not eat enough iodine is most susceptible to? a. Pheochromocytoma b. Hyperthyroidism c. Thyroid storm d. Hypothyroidism
- What is the most common cause of hyperthyroidism in the United States? a. Infection b. Corticosteroid excess c. Hashimoto’s disease d. Graves’ disease
WBC Disorders
- The Philadelphia chromosome is most commonly associated with which type of leukemia? a. CLL b. AML c. CML d. ALL
- Which of the following is NOT a manifestation of leukemia? a. Anemia b. Infection c. Weight gain d. Platelet dysfunction
- What virus is associated with the development of lymphomas? a. Epstein-Barr virus b. Influenza virus c. Varicella-Zoster virus d. Hepatitis B virus
- ALL incidence is increased in? a. Adults older than 50 y/o b. Children older than 10 y/o c. Adults younger than 50 y/o d. Children younger than 10 y/o
- Which of the following is NOT a manifestation of lymphoma? a. Night sweats b. Fever c. Bradycardia d. Painless lymph node swelling
Bleeding Disorders
- Secondary thrombocytopenia is a condition in which there is a defect in platelet production. All of the
