exam 2

Question 1

1. What are the causes of type 1 diabetes?
2. What are the causes of type 2 diabetes?
3. Where is insulin produced?
4. What is insulin’s job?

Answer 1

1. Can be genetic (but this is mostly for type 2), autoimmune destruction of beta cells, cold climate, viruses, solid food early vs breast milk.
2. genetics, obesity
3. produced by beta cells in the islets of langerhans in the pancreas
4. lowers blood sugar and stabilizes glucose range between 70-120

Question 2

1. What are the mechanisms of diabetes type 1 (just 1)

2. What are mechanisms of diabetes type 2 (describe which organs are the culprits and goes wrong at each organ):

Answer 2

1. no production of insulin due to destruction of beta cells.
2. Pancreas: defective b-cell secretion, insulin resistance stimulates more secretion leading to b-cell exhaustion.

Liver: excess glucose production, or inappropriate regulation of glucose production.

Muscle: defective insulin receptors, insulin resistance, decreased cellular uptake of glucose.

Adipose Tissue: decreased adiponectin and increased leptin result in altered glucose and fat metabolism.

Question 3

1. What does insulin do (5)?

Answer 3

1. promotes glucose transport from blood into cells, storage of glucose as glycogen, inhibits gluconeogenesis (in liver), enhances fat deposition, increases protein synthesis.

Question 4

1. What are the manifestations of diabetes type 1?
2. What are the manifestations of type 2?
3. What are the risk factors of diabetes type 2 NIDDM? Do some ethnicities have higher incidence? Which?
4. What comprises metabolic syndrome?
5. What is the signifigance of metabolic syndrome?

Answer 4

1. 3 P’s (polydipsia, polyuria, polyphagia), weight loss. Infections, fatigue
2. 3 P’s and weigh loss are possible but less prevalent than type 1. Fatigue, recurrent infections like candida, prolonged wound healing, visual changes (often the 1st sign).
3. overweight, obesity (biggest risk factor), advanced age, family history, bad eating, lack of exercise. Blacks, hispanics, asian, pacific islanders, native americans.
4. A person having 3 of the following 5 has metabolic syndrome: belly fat, high triglycerides, elevated BP, high blood sugar, low HDLs.
5. People w/ metabolic syndrome are increased risk of type 2, but this can be reversed through diet and exercise.

Question 5

1. What is the gold standard test for diabetes?
2. What is A1C a measure of?
3. What is prediabetes and what is the range of A1C for prediabetes?

Answer 5

1. A1C
2. A measure of how much sugar is stuck to hgb
3. Prediabetes is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. It has an A1C range of: < 5.7% = normal, 5.7 - 6.5 = prediabetes, > 6.5% = diabetes

Question 6

1. Which women have an increased risk for developing GDM? When do we screen high risk patients? When do we screen all others?
2. For patients who develop GDM, when does their blood glucose return to normal?
3. What percentage of GDM patients develop type 2 diabetes within 10 years of GDM?

Answer 6

1. Obese, advanced age, and maternal hx of GDM. First prenatal visit. Screen others at 24-28 weeks.
2. 6 weeks after delivery.
3. 35%-60% (50%)

Question 7

1. What are the methods of testing for diabetes?

Answer 7

1. Any of the following must be checked twice:

HGB A1C 6.5% (reflects past 2-3 mos). Good to diagnose and monitor. (7% is acceptable for diabetic)

Fasting plasma glucose higher than 126 (8 hours of fasting prior)

2 hour plasma glucose level during OGTT: 200w/ glucose load of 75g

Calssic symptoms of hyperglycemia (3P’s) with random glucose level of 200 or higher

Fructosamine (reflects glucose levels for past 2-3 weeks)

Antibodies

Question 8

1. Why do diabetics often have protein in urine?
2. Do diabetics often have glucosuria?
3. Why might a diabetic have heart problems, like ventricular hypertrophy?

Answer 8

1. Reflects kidney damage from chronic high levels of serum glucose.
2. Yes. This is the kidney’s way of trying to rid the body of glucose.
3. Damage to coronary and systemic vasculature, leading to atherosclerosis and diminished blood flow.

Question 9

1. What do we teach diabetics?
2. Do all type 1 diabetics need insulin? Type 2?
3. When diabetic patients get sick, what is their risk and what should we do?

Answer 9

1. nutrition, exercise (makes muscle cell receptors more susceptible to insulin), drug therapy, self-monitoring of glucose, foot care.
2. yes. Sometimes type 2 can be managed w/ diet and exercise.
3. changes in blood glucose levels. They can be hyperglycemic or hypoglycemic. Check blood glucose levels every 2-4 hours.

Question 10

1. Name a few rapid acting insulins w/ their onset of action, peak, and duration:
2. Name a few short acting insulins w/ their onset of action, peak, and duration:
3. Name a few intermediate acting insulins w/ their onset of action, peak, and duration:
4. Name a few long acting insulins w/ their onset of action, peak, and duration:
5. Why is it so important to know the peak times of these meds?

Answer 10

1. Rapid: lispro (Humalog), aspart (Novolog), glulisine (Apidra) onset: 10-30min, peak: 30min-3hr, duration 3-5hr.
2. Short: regular insulin (Humulin R., Novolin R): onset: 30m-1hr, peak: 2-5hr, duration: 5-8hr
3. intermediate: NPH (Humulin N., Novolin N.) onset: 1.5-4hr, peak: 4-12hr, duration: 12-18hr
4. Long Acting: glargine (Lantus), detemir (Levemir): onset: 0.8-4 hr, peak: no peak, duration: 24+hr
5. Because that is the most likely moment for a patient to have a hypoglycemic moment

Question 11

1. how long can the brain go without O2 and glucose?
2. What type of insulin is safest?
3. What are signs of hypoglycemia?
4. What is a basal bolus regimen?
5. What is the goal of basal bolus insulin?
6. Insulins that end in “log” are which type? Why are these so convenient?
7. What is one important thing to remember about long-acting insulins?

Answer 11

1. 5min
2. long acting b/c no peak
3. confusion, diaphoresis, shakiness, hunger, irritable, possibility of seizures
4. closely mimics endogenous insulin production, give a “bolus” (rapid or short acting) right before meals, and intermediate or long-acting background insulin (the “basal” part) once or twice per day.
5. to achieve near-normal glucose of 70-130 before meals
6. rapid acting. convenient because they kick in quick.
7. don’t mix long-acting with other insulins or solutions

Question 12

1. which kind of insulin is most likely to cause hypoglycemia?
2. What is the abbreviation for intermediate acting insulin? Can it be mixed with other insulins in same syringe?
3. Is intermediate insulin also considered “basal”? What does it look like?
4. Nowadays we use premixed insulin pens. But if we need to mix, briefly outline the steps:

Answer 12

1. short-acting because it has a longer duration. Also easy to make a mistake because it needs to be administered 30-45 min before a meal, which can be tricky to coordinate.
2. NPH. yes, w/ rapid or short acting.
3. Yes. Cloudy.
4. gently rotate NPH insulin to mix. Inject air into NPH. Inject air into regular insulin. Draw up regular insulin. Draw up NPH. (remember to draw up in this order: RN (regular, NPH).

Question 13

1. How do we store insulin
2. Preferred injection sites in order: Do we always inject in the same place?
3. Benefits of insulin pumps: Drawbacks:

Answer 13

1. Do not heat/freeze. Keep room temp out of sun/heat/cold. Prefilled can be kept up to 1 week if mixed. If unmixed, can be 30days.
2. abdomen, arm next, buttock next. Don’t inject in an area you’ll be exercising (ie: thigh before bike ride). Always inject in same area, but rotate sites in that area.
3. tight glucose control but can malfunction due to kinked tube etc.

Question 14

1. Problems w/ insulin therapy in order:
2. What is the somogyi effect?
3. How can we know if it is somogyi and how to avoid?
4. What is Dawn phenomenon, and how do we avoid it?
5. What is the difference between dawn and somogyi?

Answer 14

1. hypoglycemia, allergic reaction, lipodystrophy (atrophy of subcutaneous tissue/ use of human insulin helps), and somogyi effect
2. Phenomena that presents as hyperglycemia in the morning. Caused by a high dose of insulin given at night. The body attempts to counterregulate which causes morning hyperglycemia.
3. patient will report headaches, night sweats, nightmares. Try to check glucose levels between 2-4am for hypoglycemia (<60). If hypoglycemia is present, reduction in dose of insulin or a bedtime snack will help.
4. Morning hyperglycemia that happens due to growth hormone. Check glucose at 3am. If high, then it is the Dawn effect. To avoid this, limit bedtime snacks, take a walk after dinner.
5. In Dawn, there is no nocturnal hypoglycemia. In somogyi there is.

Question 15

1. In what 3 ways do diabetic type 2 oral agents work?
2. What is Metformin (Glucophage), what class of medication is it, and what is its main action?
3. What beneficial side effect does Metformin (Glucophage) have? Can it be used for pre-diabetic patients to prevent type 2?
4. What important nursing intervention must we remember with Metformin (Glucophage)?
5. What are the contraindications of Metformin(Glucophage)? What level must we check?
6. What is a rare complication of Metformin (Glucophage)? Overall though, does Metformin (Glucophage) cause other side effects? Does it cause hypoglycemia?

Answer 15

1. they work on insulin resistance, increase insulin production, and decrease hepatic glucose production.
2. An oral agent to treat type 2. It is a Biguanide. Its main action is reduction of glucose production in liver. Also improves glucose transport and insulin sensitivity.
3. weight loss. Yes.
4. Must stop 48 hours prior to procedures using contrast medium.
5. Renal, liver, or cardiac disease, and excessive alcohol intake. Check creatinine. This drug is nephrotoxic.
6. lactic acidosis. Not many side effects. No hypoglycemia.

Question 16

1. Name the drugs in the sulfonyureas:
2. How do the sulfonureas work, and what do they treat?
3. What is the major adverse effect of these drugs?
4. Name a few other oral type 2 agents:

Answer 16

1. glipizide (Glucotrol), Glyburide (Micronase, Diabeta, Glynase), and glimepiride (Amaryl).
2. Type 2 diabetes. Increase insulin production from the pancreas.
3. Can cause hypoglycemia.
4. Thiazolidinediones TZD, DDP-4 inhibitors, GLP-1 receptor agonists, SGLT2s

Question 17

1. What do we want to emphasize to our type 2 patients regarding nutrition and weight?
2. How much exercise do we need per week?
3. What do we tell athletes who are using insulin
4. when should a diabetic not exercise?

Answer 17

1. achieving healthy glucose, lipid, and BP. Weight loss (of 5-7%) also helps because it increases insulin sensitivity.
2. 150 min (3 x’s per week resistance)
3. monitor blood sugar throughout exercise (even up to 48 hours after), exercise 1 hour after eating, keep a snack handy, possible less insulin.
4. If blood glucose is >300 and if ketones are present in urine. Hyperglycemia

Question 18

1. when do we test blood glucose?
2. Which patients are candidates for pancreas transplants?
3. What is the goal with pancreas transplants?
4. Can we just transplant islet cells?

Answer 18

1. Before meals (to determine bolus), 2 hours after (to determine accuracy of bolus), if hypoglycemia is suspected, when sick, before/during/after exercise
2. type 1, already getting a kidney transplant (rare if done alone), hx of severe acute problems like ketoacidosis, problems w/ insulin administration, consistent failure of insulin-based management.
3. no more exogenous insulin (will need lifelong immunosuppressants).
4. Yes, but still experimental.

Question 19

1. What objective physical (not lab values) findings would we see in diabetic patients re eyes, skin, mouth, feet, reflexes, cognition, and musculoskeletal (15)?
2. What objective findings (physical and labs) indicate diabetic ketoacidosis (10)?
3. What are the cardiac manifestations of DKA?

Answer 19

1. sunken eyeballs, vitreal hemorrhages, cataracts, dry/warm/pigmented skin, pigmented lesions, ulcers, loss of hair on toes, acanthosis nigricans, dry mouth, vomiting, altered reflexes, confusion, stupor, coma, muscle wasting.
2. kussmaul respirations, fruity breath, dehydration, lethargy/weakness, sunken eyes, dry, loose skin. anorexia/nausea/vomiting, blood glucose >250, pH <7.3, HC03<16, ketones in urine
3. Hypotension, rapid, weak HR and pulse

Question 20

1. what findings might appear on labs (10)?
2. Name the 4 key goals in planning for our diabetic patients:
3. Which 2 areas of the body require extra attention in diabetics?

Answer 20

1. electrolyte abnormalities, Fasting blood glucose >126,
Oral glucose tolerance or random glucose >200 
Leukocytosis
↑ BUN and creatinine,
↑ Triglycerides, LDL, VLDL
↓ HDL
A1C >6.5%
Glycosuria/Ketonuria/Albuminuria
Acidosis

2. *Active patient participation
   * Establish individualized goals for teaching
   * Include family and caregivers
   * Few or no episodes of acute hyperglycemic emergencies or hypoglycemia
3. oral care and foot care

Question 21

1. What are the 3 acute metabolic conditions that can arise with diabetics and a brief explanation of each:

Answer 21

1. Diabetic Ketoacidosis: no insulin at all, typically type 1.

Hyperosmolar hyperglycemic syndrome (HHS): a little bit of insulin, type 2

Hypoglycemia

Question 22

1. What 6 factors can trigger DKA?
2. What are the nursing interventions for DKA?
3. How do we prime IV tubing when administering insulin?

Answer 22

1. Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1
Poor self-management
Neglect

2. airway/O2,
   Establish IV, start fluids (NaCl, 0.45% or 0.9%, hypotonic to pull glucose out of blood)
   Add 5% to 10% dextrose when blood glucose level approaches 250 mg/dL
   Continuous regular insulin drip,
   K+ replacement as needed
3. prime with insulin rather than NaCl so dose of insulin arrives faster to patient.

Question 23

1. What can percipitate HHS?
2. Is it more or less common than DKA? Who does it normally happen to? Is there a high mortality rate?
3. Does it present with neurological symptoms?
4. Are there ketones in blood and urine?
5. Is the therapy similar to DKA? Does it require more fluid replacement? Is the risk of hypokalemia as severe in HHS as DKA?
6. What needs to be assessed in these patients?
7. Once the patient is stabilized, what must we do?

Answer 23

1. UTIs, pneumonia, sepsis
   Acute illness
   Newly diagnosed type 2 diabetes
   Impaired thirst sensation and/or inability to replace fluids
2. less common. Happens to older adults w type 2. High mortality rate
3. Yes
4. usually not, if there are, it’s minimal.
5. Yes. Yes (but do this slowly to avoid overload). Hypokalemia is less of a risk in HHS, but still prevalent.
6. vitals, I&O, skin turgor, labs, cardiac, renal, and mental status.
7. correct the underlying cause of the problem.

Question 24

1. How do we define hypoglycemia? What is the numeric value?
2. What happens when blood glucose drops below 70?
3. What are the symptoms of hypoglycemia?
4. What causes hypoglycemia?
5. How do we proceed when a patient presents with hypoglycemic symptoms?
6. What is the treatment of hypoglycemia (rule of 15)?
7. How do you treat in a hospital if patient isn’t alert to swallow?

Answer 24

1. too much insulin in proportion to available glucose in the blood, <70
2. neuroendocrine hormones are released, activating the ANS. Symptoms begin.
3. headache, ringing in ears, trembling, irritability, sweatiness, blurry vision, increased HR, hunger, anxiety, weak and tired, altered mental functioning (early signs)
4. Too much insulin or oral hypoglycemic agents
   Too little food
   Delaying time of eating
   Too much exercise
5. Check blood glucose level, <70 start treating, >70 monitor for other possible cause. If monitoring equipment not available, start treatment.
6. Consume 15 g of a simple carbs ( 4-6oz juice/soda is best)
   Recheck glucose level in 15 minutes
   Repeat if still less than 70 gm/dL
   Avoid foods with fat (this slows absorption of sugar)
   Decrease absorption of sugar
   Avoid overtreatment
   Give complex carbs after recovery
7. Fifty percent dextrose, 20 to 50 mL, IV push, of Glucagon, 1 mg, IM or subcutaneously

Question 25

1. What are some chronic complications of diabetes?
2. Can MIs be painless due to autonomic neuropathy?
3. In men, which is one of the first manifestations of autonomic neuropathy? What can women experience? What is a sexual problem for both sexes?
4. What happens in a neurogenic bladder?

Answer 25

1. Aoutonomic neuropathy which affects all body systems:
   strokes, HTN, dermopathy, atherosclerosis, neuropathy, peripheral neuropathy, neurogenic bladder, erectile dysfunction, gangrene, peripheral vascular atherosclerosis, islet cell loss, gastroparesis, CAD, retnopathy, cataracts, glaucoma, blindness
2. yes
3. ED. vaginal infections, decreased libido
4. loss of sensation results in urinary retention. May need to do crede’s manuever (downward massage over bladder) or patient may need to learn to self-catheterize.

Question 26

1. What chronic foot problems occur?
2. Because the primary risk factor for amputations is LOPS (loss of protective sensation), what must we do on an annual basis?
3. What leads to the development of PAD? How does PAD lead to amputations? What are the symptoms of PAD?

Answer 26

1. sensory neuropathy, peripheral artery disease, clotting abnormalities, LOPS (loos of protective sensation)
2. microfilament test for sensation
3. Diabetes causing atherosclerosis (PAD is atherosclerosis in peripheral arteries). Blood flow is insufficient. pain with use of legs (intermittent claudication), relief when legs dangle, cold feet, loss of hair, delayed cap refill, rubor after dangling

Question 27

1. What does diabetic dermopathy look like?
2. What does athancosis nigricans look like?
3. What challenge do elderly people have in regard to glucose control?
4. What is the best treatment for elderly and why?

Answer 27

1. reddish-brown oval patches on legs, arms, feet, trunk
2. velvety light brown or black skin thickening on areas that flex and the back of the neck.
3. They are unaware when they are they are close to hypoglycemia
4. diet and exercise because metabolism of oral agents may be altered

Question 28

1. Trace the blood flow through the heart
2. Name the 2 Left coronary artery branches and what they serve:
3. What do the R coronary artery branches serve:
4. What drains into the coronary sinus?

Answer 28

1. superior and infecrior vena cave to R atrium. Passes though tricuspid valve to R ventricle. Next through pulmonic artery to lungs. Pulmonc veins to L atrium, through mitral valve to left ventricle to aortic valve out to body.
2. L anterior descending and L circumflex. Supply blood to L atrium and Ventricle, interventricular septum and part of R ventricle.
3. R atrium, R ventricle, part of posterior left ventricle, AV node and bundle of His
4. the coronary veins

Question 29

1. Trace the heart conduction system:
2. What do the different waves mean on the electrocardiogram?
3. What might a big U wave mean?
4. What do the intervals between waves mean, and what do changes in these intervals indicate?

Answer 29

1. SA node to AV node to bundle of HIS. Next to R and L bundle branches and down to the purkinje fibers.
2. P = firing of SA and atrial depolarization
   QRS = depolarization of AV node and ventricles
   T = repolarization of ventricles.
   U = repolarization of purkinje fibers (may not be seen)
3. possibly hypokalemia
4. time of impulse travel from one area of the heart to another. Changes may mean pathologic conditions.

Question 30

1. What is the leading cause of death in adults over 65?
2. What is CAD?
3. Name a few things that happen to older adults in regard to their circulation, re: systolic BP, venous return, orthostatics, and kyphosis:
4. What happens to collagen and elastin and what does it lead to?
5. T or F, heart valves become stiff and cause murmurs?
6. What happens with pacemaker cells and what is the effect?
7. What happens to beta adrenergic receptors (beta 1)?

Answer 30

1. CVD
2. Coronary artery disease, the most common type of CVD that comes from atheroscelrosis.
3. Vessels thicken causing increase in systolic BP but not diastolic. (need more pressure to perfuse)
   Venous valves become incompetent leading to dependent edema.
   orthostatic hypotension becomes common, particularily after meals, leading to falls. Kyphosis doesn’t allow for proper lung expansion.
4. increased collagen and decreased elastic leads to myocardial hypertrophy
5. T
6. They decrease, leading to dysrhythmias and heart block
7. they decrease in number causing a decreased stress response and decreased response to stimulus.

Question 31

1. Which type of drugs are African Americans less receptive to? Use what instead?
2. Which is more dangerous, arrhythmias or dysrhythmias?
3. What are the safe levels of the following: Total cholesterol, HDL, LDL, Triglycerides.
4. What kind of angina does CAD cause? What kind of angina does Acute coronary syndrome cause? How does ACS differ from CAD?
5. When we talk about “hardening of arteries” (thik general, all arteries), what disease are we referring to?
6. When we develop atheromas in the coronary arteries, what is it called?

Answer 31

1. ACE inhibitors. Use diuretics
2. dysrhythmias.
3. Total cholesterol: <200
   HDL: >40
   LDL: <130
   Triglycerides: <150
4. CAD: asymptomatic or chronic stable angina.
   ACS: unstable angina (UA) or myocardial infarction (MI). Both CAD and ACS are types of CVD, but ACS involves a larger clot that can completely occlude.
5. Atherosclerosis.
6. CAD

Question 32

1. Chronic stable angina =
2. Unstable angina =
3. Non-STEMI =
4. STEMI =
5. what is a tobmbstone?

Answer 32

1. Chronic stable angina = only ischemia
2. Unstable angina = partial thrombus occlusion, non-specific ECG, normal cardiac enzymes
3. Non-STEMI = occluding thrombus causes tissue necrosis, elevated cardiac enzymes – may see ECG changes but not ST elevation
4. Complete thrombus occlusion causing infarction of the tissue, will see ST elevation or LBBB (left bundle branch block), elevated cardiac enzymes
5. ST elevation MI.

Question 33

1. What does Nitro do? Name a common side effect. What med can’t be mixed with this? Does it need to be kept in the dark?
2. What is Prinzmetal angina and how does it differ from other types of angina?
3. What are some common causes of Prinzmetal angina, and what meds treat?
4. What are the goals in treating angina, and what drug achieves this?

Answer 33

1. It causes vasodilation. Headache. Sidenafil (Viagra). Keep in dark
2. Coronary spasm that happens at rest
3. Vasoconstricting meds, Cold, stress, smoking, drugs (weed and coke), exercise. Treat with calcium channel blockers and nitro.
4. Decreasing O2 demand while increasing O2 supply. Nitro and rest.

Question 34

1. What is the main lab value to look at to determine MI as well as the normal level.
2. What is the difference between troponin i or t?
3. What lab must be known before going to cath lab?
4. What test would you expect if you presented with chest pain? Does this test rule out an MI?
5. Aside from Troponin, name a few other labs that could be drawn for suspected MI?

Answer 34

1. Troponin I (<0.2) or T (<0.03).
2. I shows levels from 3-5 hours whereas T shows levels after 3 hours up to 14 days.
3. Creatinine
4. 12-lead. DOESNT rule out MI
5. Creatine Kinase MB, Myoglobin, and CRP - measure of inflammation. Elevated in MI

Question 35

1. What are the symptoms of an MI?
2. What is a transmural MI?
3. How long does it take for the full thickness of myocardium to become necrotic?
4. How long can we have sustained ischemia before irreversible myocardial cell death occurs?
5. T or F, most MIs involve the L ventricle?

Answer 35

1. Sudden onset of substernal pain, crushing, tightness, unrelieved by nitro, may radiate to back, neck, jaw, shoulder, or arm, dyspnea, syncope (passing out), nausea, vomiting, extreme weakness, diaphoresis, denial, increased HR
2. full thickness MI
3. 4-6 hours. >20min
4. > 20 minutes
5. T

Question 36

1. What is the most common complication resulting from an MI
2. Name some other complications post MI (6)
3. What is the gold standard treatment of MI?
4. Name a few other treatments for MI:

Answer 36

1. Dysrhythmias
2. Heart failure
   Cardiogenic shock
   Papillary muscle dysfunction – if MI is near mitral valve
   Ventricular aneurysm
   Acute pericarditis
   Dressler syndrome – pericarditis and fever 1-8 weeks post MI
3. Angioplasty (PTCA) to place stent
4. Thromolytics (best given within 2 hours of symptoms, but can be given up to 12 hours), Coronary Artery Graft Bypass (CABG), other meds.

Question 37

1. What must we do to prep our patient for an angioplasty (7)?
2. What are 4 priorities we do for our patient post procedure?
3. what does MONA mean and stand for?
4. What are thromblytics and name the main one. Also what is the time window to give for MI treatment?

Answer 37

1. consent form, NPO, assess for iodine or shellfish alllergy, admin of sedatives and analgesics (versed, a benzo), assess creatine levels (to see if kidneys can tolerate contrast), stop heparin, monitor patient
2. assess groin for bleeding, assess pedal pulse color temp, bedrest (flat) 4-6 hours,
3. Acronym for treatment of MI type symptoms in ER. Morphine, O2, Nitro, Aspirin
4. Drugs that dissolve clots. TNK (tenecteplase). Give btw 4-6 of MI. NOT AFTER

Question 38

1. What are the preventative measure for DVTs?
2. What lab do we watch with heparin, and what are therapeutic heparin levels?
3. What do we watch for with coumadin as far as labs and adverse reactions?
4. Name 2 other anticoagulants

Answer 38

1. Keep the patient moving
Range of motion 
Passive or active 
 Meds after high risk procedures and surgeries i.e., enoxaparin (Lovenox), apixaban 
Surgical compression device & TED hose 
Hydrate 
semi-fowler

2. aPTT 1.5-2 x’s normal (norm is 21-35sec). Watch for bleeding
3. monitor PT/*INR (INR 2-3)
   watch for bleeding AND food/drug interactions
4. apixaban and rivaroxaban

Question 39

1. What is the greatest risk of DVTs? and which kind is the worst, causing sudden death?
2. Name some symptoms of DVT
3. Name some symptoms of PE
4. How can we diagnose PE
5. what are the risk factors to DVT?

Answer 39

1. pulmonary emolus. Saddle embolus worst
2. cramping, swelling, pain, red, warm
3. anxiety, pressure in chest, pain w/ inspiration, exertional dyspnea, cough, tachycardia, tachypnea, hypotension, pale/cyanotic color, diaphoresis
4. with a cat scan
5. Immobility for any reason, estrogen, tobacco, dehydration, obesity, old, a-fib, contraceptives, pregnancy, long bone fracture, hip/knee arthplasty

Question 40

1. What is the risk in a-fib?

2. If a clot forms in R heart, where would it go? L heart?

Answer 40

1. blood pooling an forming clots

2. lungs. brain

Question 41

1. Which bleeding time test is used for coumadin?
2. Which bleed time test is used for heparin?
3. Describe how metoprolol covers hypoglycemia:
4. If your hypoglycemic patient is unconscious, how do you treat them (in hospital and out)?

Answer 41

1. INR
2. aPTT
3. One sign of hypoglycemia is increased HR. Metoprolol forces HR to be slower. So, diabetics w/ hypoglycemia may not see their HR increase.
4. IN hospital, give D50 w/ IV access. If no IV access, give glucagon IM.

Question 42

1. Which gene may determine BMI?
2. What does neuropeptide Y do?
3. What does Leptin do?
4. What does Ghrelin do?

Answer 42

1. FTO gene
2. its a powerful appetite stimulant
3. suppresses appetite and increases fat metabolism
4. It inhibits Leptin

Question 43

1. At which BMI is someone considered obese?
2. At which BMI do we begin drug therapy and behavior modification?
3. Which treatment is most successful (gold standard) for long term treatment of obesity?
4. What are the 3 types of bariatric surgery? Name the most common in US:
5. Name a short term complication of bariatric surgery: Name a few long term complications:
6. When obese patients have surgery they are likely to suffer from which other comorbidities?

Answer 43

1. > 30
2. > 30 or 27 if there are coexisting medical conditions related to weight.
3. bariatric surgery
4. restrictive (size of stomach os reduced), malabsorptive (length of small intestine is shortened), combination of both. Route en Y is most common in US
5. short term: wound infections. Long term: anemia, vitamin deficiencies, diarrhea, psychosocial problems

6. Diabetes
Altered cardiorespiratory function
Abnormal metabolic function
Hemostasis (blood pooling)
Atherosclerosis

Question 44

1. What pre-op measures should nurses take to prepare for patients undergoing bariatric surgery?
2. What might we have the patient practice prior to surgery?
3. What might we teach bariatric patients about their diet?
4. What do we do post op? What do we need to assess for with the anastamosis?
5. What is the significance of extra adipose tissue on the breathing status of post op patients?

Answer 44

1. prep room w/ larger BP cuff, larger gown, patient transfer equipment (like wheelchair w removeable arms). Longer IV catheters
2. practice coughing, spirometer, turning/repositioning, splinting chest and abdomen.
3. May need additional vitamins (i.e., calcium, cobalamin, A, D, E), limit fats/carbs and increase protein to avoid dumping syndrome, eat drink slowly, and drink liquid between rather than during meals.
4. elevate HOB, stabilize airway, manage pain, evaluate for re-sedation, watch for DVT, respiratory rate, and dehiscence/infection. Make sure anastamosis isn’t leaking. Pay attention to NG tube placement
5. excess adipose weighs heavy on chest and abdomen causing CO2 retention, pulmonary HTN, and polycythemia

Question 45

1. What two conditions predispose a patient to GERD?
2. What are the most common manifestations of GERD and name/describe a complication that can arise from GERD:
3. What types of drugs are used to treat GERD?
4. Long term use of proton pump inhibitors can lead to what? How to avoid problems with this drug?
5. Non-pharmacological interventions for GERD?

Answer 45

1. hiatal hernia and incompetent lower esophagus
2. Heartburn and dyspepsia
   Barrett’s esophagus (esophageal metaplasia), a precancerous lesion that increases risk for esophageal cancer.
3. Proton Pump inhibitors, Histamin receptor blockers, Antacids, and cholinergics (metoclopramide - reglan)
4. hip, wrist, spine fractures, c-diff in hospitalized patients. Take for shortest duration possible.
5. elevate HOB, don’t eat before bed, lose weight, diet/weight loss, limit smoking and alcohol, manage stress.

Question 46

1. What are the 2 types of peptic ulcer? How long after eating does each type cause pain? Does the pain occur at night? Is the pain relieved by food?
2. What causes peptic ulcers?
3. How do NSAIDs cause peptic ulcers? What can it lead to?
4. What findings can be assessed with peptic ulcers?
5. What tests or labs are done to diagnose peptic ulcer?
6. Which drugs or drug types might be given to treat peptic ulcers?

Answer 46

1. gastric: 30-60 min after eating, rarely hurts at night, exacerbated by food.
   duodenal: 1.5-3 hours ater food, occurs at night, relieved with food.
2. NSAIDs, H-pylori, stress, hypersecrtion, alcohol, and smoking
3. NSAIDs inhibit prostaglandin synthesis, increase gastric acid secretion, reduce integrity of the mucosal barrier. Can lead to renal failure
4. Epigastric pain with palpation
   Bloody emesis (hematemesis)
   Dark tarry stools (melena)
   Weight loss
5. H. pylori testing
   Hgb and Hct
   Stool for occult blood
   EGD – esophogastroduodenoscopy best dx test
6. Proton pump inhibitors (prilosec), H2 blockers (Rantinidine), antiinfectives, metronidazole (anti-ulcer and anti protozoal), carafate (GI protectant) magnesium hydroxide, pepto

Question 47

1. What is the most typical reason for a GI bleed?
2. If a peptic ulcer gets bad enough, what can it do (leading to a bleed).
3. What are the signs of perforation or hemorrhage?
4. How should we position patients with bleeding from a perforation?

Answer 47

1. Peptic ulcer
2. Perforation
3. rigid abdomen, hyperactive to diminished bowel sounds, rebound tenderness, melena, hematemesis, Tachycardia
   Low blood pressure
4. in trendelenburg or just flat. Only if not nauseated or having trouble breathing

Question 48

1. Small bowel obstuctions have a …………. onset, whereas large bowel have a ………. onset.
2. what are the risk factors for SBO
3. symptoms of sbo:
4. Diagnostics of SBO:
5. What do nurses assess in SBO?
6. Which organ may be affected by SBO and what electrolyte might be out of whack?
7. Upper obstruction =
   Lower obstruction =

Answer 48

1. faster, slower

2. Adhesions from prior surgery #1 cause
Hernia
Cancer
Strictures from Chron’s disease
paralytic ileus, lumbar/thoracic spine fractures

3. colicky pain, nausea/vomiting, abdominal distention, constipation, abdominal tenderness and rigidity
4. abdominal xray, CT, barium enema

5. Pain
Color output
Bowel function/flatus
Abd girth, tenderness
Input and output
BUN, creatinine, and KCL 

6. kidneys because may not be getting water, K+ (hypokalemia)
7. upper = vomiting and metabolic alkalosis.
   lower = diarrhea and metabolic acidosis

Question 49

1. What would vomiting around the NG tube signify?
2. What about new blood in canister?
3. What would it mean if output suddenly stopped?
4. How do you check NG tube placement?
5. Is mouthcare necessary?

Answer 49

1. tube isn’t doing its job of decompressing stomach
2. active bleeding
3. tube has been displaced
4. inject 30 ml of air or x-ray
5. YES!

Question 50

1. What are the most common causes of pancreatitis?
2. What are the 2 classifications for pancreatitis?
3. Pancreatitis symptoms:
4. What serious assessment findings should you be aware of?

Answer 50

1. biliary tract disease (in women), alcoholism (in men). Also hypertriglyceridemia. LUQ or middle radiating to back.

2. Mild pancreatitis (edematous or interstitial) 
Severe pancreatitis (necrotizing pancreatitis).

3. LUQ or epigastric pain that radiates, worse when lying down, not relieved by vomiting, nausea, vomiting, hypotension, tachycardia, jaundice
4. Internal bleeding presenting as Ecchymosis on the flanks (Turner’s sign)***
   Bluish discoloration of the periumbilical area (Cullen’s sign)

or

Tetany caused by hypocalcemia (this is caused by fat necrosis from enzymes)
Trusseau’s sign*
Chvostek’s sign*
Twitching of fingers, spasms

Question 51

1. What labs results can be seen with pancreatitis (note the best marker)?
2. What is the best diagnostic imaging for pancreatitis?
3. What complcations can arise from pancreatitis?
4. What are the nursing interventions for pancreatitis?
5. What test can be done to rule out cholecystitis as a cause of pancreatitis?

Answer 51

1. Lipase (best marker), amylase, increased wbcs, low Ca+ and Mg, elevated Liver enzymes, elevated blirubin, elevated glucose, decreased insulin
2. CT w/ contrast
3. pseudocyst (can rupture and hemorrhage) and abscess
4. NPO!
   Antiemetic
   Pain management (may require large amounts of opioids)
   TPN
   Limit stress, no smoking or etoh
   IV fluids (up to 6 L can be third-spaced)
   Monitor vital signs, electrolytes
   Teach to splint chest to prevent atelectasis
5. ERCP = Endoscopic Retrograde Cholangiopancreatography

Question 52

1. What drugs can be given for pancreatitis?
2. What organ would we want to listen to in pancreatitis? Why?
3. Which electrolyte can become imbalanced in pancreatitis?

Answer 52

1. Antibiotics
   Anticholinergic/antisposmodic dicyclomine (Bentyl)
   H2 blockers and PPIs
   Pancreatic enzyme called pancreatin or pancrelipase – aids in fat digestion, opioids
2. lungs for crackles due to IV fluids (since NPO)
3. calcium

Question 53

1. Cholecystitis =
2. Cholelithiasis =
3. Risk factors for gallbladder disease?
4. S/S of gallbladder disease:
5. What do urine and stools look like and why?

Answer 53

1. inflammation of the gallbladder wall
2. stones in gall bladder (bile or cholesterol turns into stones)

3. Forty
Female
Fat
Fertile 
Genetics
Older than 60
DM I (high triglycerides)
High protein, low calorie diets
Weight loss (increases cholesterol)

4. RUQ or epigastric pain that radiates to right shoulder, pain w/ inspiration, murphey’s sign (pain when palpating under right ribs), rebound tenderness, fever, dyspepsia, belching, flatulance, itching (due to leaked bile)
5. clay colored stool (bile doesn’t make it to stools), and tea colored urine (bile in urine)

Question 54

1. What are the lab findings in gall bladder disease?
2. What diagnostics may be used to diagnose gall bladder disease?
3. What are the nursing interventions for gall bladder disease?
4. What surgery might happen, and what must we do as nurses?
5. What diet education do we give to post op cholesysectomy?

Answer 54

1. increased wbcs w/ L shift, increased serum bilirubin, elevated amylase and lipase (if pancreas involved), ALT/AST elevated, increased total cholesterol
2. ultrasound (will elicit murphey’s w/ wand), xray, HIDA scan (hepatobiliary scan to see all ducts), ERCP (same as pancreas).
3. analgesics (opioids), Dicyclomine (bentyl and anti-sposmodic), bile acid to aid in digestion, benedryl or oatmeal bath for itching, IV fluids, NPO, sepsis checks, lithotripsy
4. cholesysectomy. Monitor drainage from T-tube (will be very irritating to skin), maintain flow by gravity, clamp tube 1-2 hours before and after food to assess tolerance to eating, assess for bile peritonitis, assess stool color.
5. low fat, not fried, no chocolate, lose weight, fat-soluble vitains, bile salts may be needed, small/frequent foods, avoid gassy foods (beans cabbage etc).

Question 55

1. Name the modifiable risk factors to CAD, MI, and ACS
2. Name the non-modifiable risk factors to CAD, MI, and ACS
3. What condition precludes CAD?

Answer 55

1. Total Cholesterol > 200, HDL < 40, LDL > 130, Triglycerides more than 150, tobacco use, HTN, stress, obesity, diabetes.
2. age, gender, ethnicity, family history, genetics
3. Atherosclerosis

Question 56

1. S/S of L sided heart failure:
2. S/S of R sided heart failure:
3. What are ANP and BNP and what is their role in CHF?
4. Is BNP an important lab value to look at? Why or why not?
5. What effects do prostaglandin and nitric oxide have on CHF?

Answer 56

1. Blood backs into L atrium and pools causing respiratory issues:
   dyspnea, crackls, pink-frothy sputum, pulmonary congestion and pulmonary edema
2. Usually caused by L sided heart failure. Blood backs up in veins and causes
   palpitations
   chest discomfort
   shortness of breath
   fluid retention, especially in your lower body
   weight gain
   JVD
3. Atrial and Brain naturietic peptides. They are released in response to heart muscle stretching and increased blood volume. Help in CHF by causing diuresis, vasodilation, coutering RAAS and sympathetic nervous system
4. YES! levels >100 indicate heart wall stretching, often caused by CHF
5. They cause vasodilation and decreased afterload, which is beneficial.

Question 57

1. What are the manifestations of chronic heart failure?
2. What are the early, later, and progressed manifestations of acute decompensated heart failure?
3. What is the main symptom of pulmonary edema and is this a medical emergency?
4. Drugs and treatments for chronic HF:
5. Drugs for ADHF:
6. Diet for HF:

Answer 57

1. Fatigue, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, tachycardia, palpitations, enlarged liver, edema, nocturia, skin changes, sleep probs, mental status change, chest pain, weigh gain, neuro issues
2. early: mild increase in RR, decreased spO2
   later: tachypnea, sob
   progressed: alveolar edema and respiratory acidosis
3. frothy, blood-tinged sputum. YES!!
4. O2 (or exercise if patient is doing well), RAAS inhibitors (ACE inhibitors - “pril” drugs), beta blockers, vasodilators, positive iontropes (dopamine, digitalis etc.), Corlanor (inhibits SA node). Rest frequently. Conserve energy
5. loop diuretics and vasodilators. Morphine and positive iontropes (dopamine, digitalis etc.)
6. Fluid restriction and Na+ <2g/day. Daily weights. Gain of 3lbs over 2 days, or 3-5lbs over a week needs to be reported

Question 58

1. Diseases of hyperthyroidism:
2. What is thyrotoxicosis?
3. What is Hashimoto’s disease?
4. What does the radioactive iodine uptake do?
5. What is the priority assessment for hyperthyroidism?

Answer 58

1. Graves disease, Thyroiditis, toxic nodular goiter, excess iodine, pituitary tumors, thyroid cancer
2. life threatening syndrome of hypermetabolism caused by too much T3 and T4. Usually percipitated by sickness, DKA etc.
3. It is an autoimmune disorder that attacks the thyroid, resulting in hypothyroidism.
4. used to differentiate Graves from other types of thyroiditis. Also used to kill parts or all of thyroid to limit T3 and T4
5. HTN and increased cardiac output.

Question 59

1. What is meant by primary hypothyroidism and secondary hypothyroidism?
2. What can cause hypothyroidism?

Answer 59

1. Problem exists with in thyroid gland. Has nothing to do with pituitary. You’ll see low T3 and T4, but elevated TSH

Secondary is a prob w/ pituitary and you’ll see decreased TSH as well as decreased T3 and T4

2. pituitary insufficiency, lack of iodine, meds for hyperthyriodism, other meds like amiodarone and lithium, autoimmune disorders like Hashimoto’s, removal or injury of thyroid

Question 60

1. What are the 3 main tx for hyperthyroidism?
2. Can beta blockers be used for hyperthyroid?
3. What electrolyte imbalance might happen in thyroidectomy?

Answer 60

1. antithyroid meds (PTU) and methimazole (tapizole), radioactive iodine therapy (tx of choice), and thyroidectomy
2. yes, they slow the heart
3. Hypocalcium. Check for chostek’s and trousseaus - tetany

Question 61

1. Primary hyperthyroidism is normally caused by ………….. disease, or ……………… and is a problem of too much T3 and T4 from the ……………. . Levels of TSH will be …………. .
2. Secondary hyperthyroidism is caused by a problem in the ……………, in which too much ………… is secreted.
3. Tertiary hyperthyroidism is caused by a problem in the …………….., where too much ….. is secreted.
4. What are the pharmacologic tx for hyperthyroidism?
5. What is the diet for hyperthyroidism?
6. What will we do for exopthalmus?
7. What is the life threatening complication stemming from hyperthyroidism?

Answer 61

1. Graves, toxic goiter, thyroid itself. TSH will be normal or low.
2. pituitary, TSH
3. hypothalmus, TRH
4. PTU, iodine, beta-blockers and, methimazole
5. high protein, high calorie diet
6. Tape eyes shut for sleep, and admin of artificial tears
7. thyrotoxicosis or thyroid storm