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Internal Medicine - EXAM 3 > EXAM 3 > Flashcards

EXAM 3 Flashcards

1
Q

What are the 5 general functions of the endocrine system?

A
  1. Differentiation of the reproductive and central nervous system of the
    developing fetus.
  2. Stimulation of sequential growth and development during childhood and
    adolescence.
  3. Coordination of the male and female reproductive systems.
  4. Maintenance of optimal internal environment throughout the life span.
  5. Initiation of corrective and adaptive responses when emergency demands
    occur.
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2
Q

What are 8 hormones produced by the anterior pituitary gland?

A

Somatotropin (growth hormone [GH]), Thyroid-stimulating hormone (TSH), Follicle stimulating hormone (FSH), Luteinizing hormone, Prolactin (PRL; luteotropic hormone), Adrenocorticotropic hormone (ACTH), Lipotropin (LPH), Melanocyte stimulating hormone (MSH)

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3
Q

What are the catecholamines?

A

Epinephrine, norepinephrine, and dopamine

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4
Q

What are the signs and symptoms of endocrine disease?

A

Muscle weakness, atrophy, myalgia, and fatigue

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5
Q

What are the primary hormones produced by the thyroid gland?

A

Thyroxine (T4), Triiodothyronine (T3), and Calcitonin

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6
Q

What are some more clinical manifestations of hyperthyroidism?

A

Peri-arthritis, myopathy, and respiratory muscle weakness

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7
Q

What are the major forms of therapy for hyperthyroidism?

A

Antithyroid medication, radioactive iodine (RAI), and surgery

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8
Q

What does the outer cortex secrete?

A
  1. Mineralocorticoids (steroid hormones that regulate fluid and mineral balance)
  2. Glucocorticoids (steroid hormones responsible for controlling the metabolism of glucose)
  3. Androgens (sex hormones)
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9
Q

What does the inner medulla secrete?

A

Epinephrine & Norepinephrine

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10
Q

What causes Cushing Syndrome (hypercortisolism)?

A

1) hyperfunction of the adrenal gland (usually benign or malignant
adenomas, rarely a carcinoma)
2) an excess of corticosteroid medication
3) an excess of ACTH stimulation from the pituitary gland (or other sites)

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11
Q

What are the BMI classifications?

A

Underweight: <18.5
Normal Range: 18.6 - 24.9
Overweight: 25.0 - 29.9
Obese (Class I): 30.0 - 34.9
Obese (Class II): 35.0 - 39.9
Obese (Class III): >39.9

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12
Q

What are the genes linked to obesity?

A

1) Neuropeptide Y (NPY) (stimulates the appetite)
2) Beacon 18 gene (stimulates the appetite)
3) OB gene (produces leptin - switches off the appetite)

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13
Q

What is related to (caused by?) metabolic syndrome?

A

1) Abdominal obesity
2) Atherogenic dyslipidemia
3) Elevated blood pressure
4) Insulin resistance
5) Prothrombotic and proinflammatory state of the blood

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14
Q

What do beta, alpha, and delta cells do?

A

Beta - produce and secrete insulin
Alpha - release glucagon, which then stimulates the breakdown of glycogen into glucose
Delta - release somatostatin (GH) to regulate insulin and glucagon

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15
Q

What are the values for A1c test?

A

Normal: <5.7
Prediabetic: 5.7 - 6.4
Diabetic: >6.4

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16
Q

What are the values for fasting blood sugar test?

A

Normal: <100 mg/dL
Prediabetic: 100 - 125 mg/dL
Diabetic: >125 mg/dL

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17
Q

What are the values for glucose tolerance test?

A

Normal: <140 mg/dL
Prediabetic: 140 - 199 mg/dL
Diabetic: >199 mg/dL

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18
Q

What are the effects of insulin deficiency?

A

1) Decreased utilization of glucose (also occur in early T2D)
▪ Glucosuria (sugar in the urine) and polydipsia (extremely thirsty)
2) Increased fat mobilization
▪ Produce ketones –> ketonuria and ketoacidosis
3) Impaired protein utilization
▪ Hamper the inflammatory process and diminish the tissue’s ability to repair.

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19
Q

What are symptoms of diabetes?

A

Always thirsty, weight loss, fatigue, numbness of limbs, blurred vision, frequent urination, vaginal infections, always hungry, wounds do not heal.

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20
Q

What are the type II diabetes health risks?

A

Blindness, kidney failure, heart disease, stroke, loss of toes/feet/legs

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21
Q

For diabetics, what does “control the ABC’s” mean?

A

A = A1c less than 7.0%
B = Blood pressure less than 130/80
C = Cholesterol (LDL <100 mg/dL, HDL >50 mg/dL, triglycerides <150 mg/dL)

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22
Q

What are the endogenous opioids?

A

Endorphins, Enkephalins, and Dynorphins

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23
Q

What are common strong agonist drugs?

A

➢ Hydromorphone (Hydrostat, Dilaudid)
➢ Meperidine (Demerol)
➢ Methadone (Dolophine, Methadose)
➢ Morphine (MS Contin, Roxanol, Statex, others)
➢ Tramadol (Ralivia, Ultram)

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24
Q

What are common mild-to-moderate agonist drugs?

A

➢ Codeine
➢ Hydrocodone (Hycodan)
➢ Oxycodone (OxyContin, Roxicodone)
➢ Propoxyphene (Darvon)

think “CHOP”

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25
Q

What are other opioid uses?

A

➢ Anesthetic pre-medication or as an adjunct in general anesthesia.
➢ Cough suppression (short-term use of codeine and codeine-like agents).
➢ Control of severe diarrhea.
➢ Acute pulmonary edema.

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26
Q

What are problems and adverse effects of opioids?

A

► Mental slowing and drowsiness (sedative properties)
► Respiratory depression (slow the breathing rate)
► Orthostatic hypotension
► GI distress

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27
Q

What are physical withdrawal symptoms?

A

Body aches, diarrhea, fever, gooseflesh, insomnia, irritability, loss of appetite, nausea/vomiting, runny nose, shivering, sneezing, stomach cramps, sweating, tachycardia, uncontrollable yawning, weakness/fatigue

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28
Q

What are the more apparent changes in the endocrine system as we age?

A

Glucose homeostasis, reproductive function, and calcium metabolism

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29
Q

What contributes to the neuroendocrine response to stress?

A

Catecholamines, Cortisol, Endorphins, GH, Testosterone, Prolactin

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30
Q

What causes hypo/hyper-function in the endocrine system?

A

1) inflammation
2) tumor(s) in hypothalamus, pituitary gland, and/or other endocrine glands

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31
Q

Adipose tissue secretes hormones responsible for _____________.

A

1) metabolism
2) hunger
3) vasoconstriction
4) cellular growth and development

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32
Q

Carpal tunnel syndrome (CTS) is a common finding in people with certain endocrine/metabolic conditions such as ______________________.

A

1) acromegaly
2) diabetes
3) pregnancy
4) hypothyroidism

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33
Q

Anterior Pituitary = _____________

Posterior Pituitary = _____________

A

Adenohypophysis - Neurohypophysis

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34
Q

What does acromegaly look like?

A

coarsened facial features; protrusion of the jaw (prognathism); thickened ears, nose, and tongue; and broad hands, with spade-like fingers

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35
Q

What are the primary hormones produced by the thyroid?

A

Thyroxine (T4), Triiodothyronine (T3), and Calcitonin

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36
Q

What anatomic abnormalities may come from disorders of the thyroid gland?

A

1) thyroiditis (Hashimoto disease - infected glands)
2) goiter (result of excess TSH)
3) tumor

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37
Q

Hyperthyroidism = __________________

A

Thyrotoxicosis

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38
Q

What is “thyroid storm” characterized by?

A

1) high fever
2) severe tachycardia
3) delirium
4) dehydration
5) extreme irritability or agitation

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39
Q

What are clinical manifestations of hyperthyroidism?

A

1) mild symmetric enlargement of the thyroid (goiter)
2) nervousness
3) heat intolerance
4) weight loss despite increased appetite
5) sweating
6) diarrhea
7) tremor and palpitations

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40
Q

“Protruding Eyes” = _____________

A

Exophthalmos

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41
Q

__________________ with stiffness is a common finding in persons with __________________.

A

Flexor tenosynovitis - hypothyroidism

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42
Q

Pituitary Gland = ______________ & ________________

A

hypophysis - “master gland”

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43
Q

____________ lobe disorders are more common than ____________ lobe disorders.

A

Anterior - Posterior

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44
Q

Both T3 and T4 regulate the _______________________ and _______________________.

A

metabolic rate of the body - increase
protein synthesis

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45
Q

Calcitonin has a weak physiologic effect on _____________ and _____________ balance in the body.

A

calcium - phosphorus

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46
Q

What are the functional abnormalities of the thyroid gland?

A

hyperthyroidism and hypothyroidism

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47
Q

What creates a generalized elevation of body metabolism?

A

hyperthyroidism

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48
Q

What is the most common form of hyperthyroidism?

A

Graves Disease (increases T4 production)

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49
Q

What are some stressors of hyperthyroidism?

A

1) surgery
2) infection
3) toxemia of pregnancy
4) labor and delivery
5) diabetic ketoacidosis (DKA)
6) myocardial infarction
7) pulmonary embolus
8) medication overdose

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50
Q

Who are the “culprits” in Graves Disease?

A

thyroid-stimulating immunoglobulins (TSIs)

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51
Q

If a patient has hyperthyroidism and gets a lab test done, what levels will be shown for TSH and antithyroid antibodies (like TSIs)?

A

TSH = low ….. TSI’s = high

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52
Q

When it comes to hyperthyroidism, what requires a medical referral?

A

1) unusual swelling
2) enlargement with or without symptoms of pain
3) tenderness
4) hoarseness
5) dysphagia (difficulty swallowing)

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53
Q

What are some side effects of radioiodine therapy?

A

everyone who receives RAI becomes hypothyroid (for the first year) and requires thyroid hormone replacement for the rest of their lives…the hypothyroid issue eventually normalizes with therapy

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54
Q

What results in a generalized slowed body metabolism (basal metabolic rate)?

A

hypothyroidism

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55
Q

Type I /primary hypothyroidism = _____________

Type II / secondary hypothyroidism = _____________

A

hormone deficient (hormones not produced)

hormone resistant (not receiving enough TSH from pituitary gland)

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56
Q

Hypothyroidism leads to _____________________________.

A

1) bradycardia
2) decreased GI tract motility
3) slowed neurologic functioning
4) decrease in body heat production
5) achlorhydria

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57
Q

Lipid metabolism is altered in hypothyroidism, leading to an ____________ in ____________ and _____________.

A

increase – serum CHOLESTEROL – TRIGLYCERIDE levels

(think of FAT)

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58
Q

What is myxedema?

A

Nonpitting, boggy edema, especially around the eyes, hands, feet, and in the supraclavicular fossae

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59
Q

What are some clinical manifestations of hypothyroidism?

A

1) myxedema
2) flexor tenosynovitis (CTS)
3) myopathy
4) delayed relaxation time
5) Rheumatic symptoms
6) fibromyalgia
7) inflammatory arthritis on small joints

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60
Q

TSH levels are always __________ in _______________.

A

elevated – primary hypothyroidism

(TSH is “pumping” nonstop, but to no avail b/c the thyroid gland is deficient)

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61
Q

What is calcium pyrophosphate deposition disease (CPPD) associated with?

A

hypothyroidism

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62
Q

What are all the pressure points to be aware of?

A

1) sacrum
2) coccyx
3) scapulae
4) elbows
5) greater trochanter
6) heels
7) malleoli

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63
Q

After “addressing” _____________, you should “watch” for _____________.

A

hyperthyroidism – hypothyroidism

OR

hypothyroidism – hyperthyroidism

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64
Q

Exercise-induced myalgia could lead to ________________.

A

rhabdomyolysis (damaged muscle tissue releases proteins and electrolytes, especially myoglobin, into the bloodstream)

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65
Q

Parathyroid glands secrete _________, which regulates __________________________.

A

PTH – calcium and phosphorus metabolism

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66
Q

What does PTH do?

A
  1. Increases the release of calcium and phosphate from the bone (bone
    demineralization).
  2. Increases the absorption of calcium and excretion of phosphate by the kidneys.
  3. Promotes calcium absorption in the GI tract.
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67
Q

What are the characteristics of hyperparathyroidism?

A

1) increased bone resorption
2) elevated serum calcium levels
3) hypercalciuria and hyperphosphaturia
4) depressed serum phosphate levels (b/c of high excretion in kidneys)
5) decreased neuromuscular irritability

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68
Q

What are the characteristics of hypoparathyroidism?

A

1) decreased bone resorption
2) depressed serum calcium levels
3) hypocalciuria and hypophosphaturia
4) elevated serum phosphate levels (b/c of low excretion in kidneys)
5) increased neuromuscular irritability

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69
Q

What do endogenous opioid peptides do?

A

1) control pain and inflammation

2) regulate the immune system

3) regulate gastrointestinal (GI) function

4) regulate cardiovascular responses

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70
Q

Endogenous opioid peptides are involved in many aspects of behavior, including _________________.

A

1) response to physical and psychological stress

2) eating and drinking behaviors

3) physiological addiction to exogenous opioids and other drugs

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71
Q

What are the 3 opioid receptors?

A

Mu(µ1-3), Kappa (κ1,2), and Delta (δ1-3)

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72
Q

What is a strength (pro) of mixed agonist-antagonists?

A

Less risk of the side effects associated with mu receptors.

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73
Q

What is a weakness (con) of mixed agonist-antagonists?

A

1) May produce more psychotropic effects.

2) Maximal analgesic effect may not be as great as strong mu agonists.

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74
Q

Glucocorticoids = ________________

A

Cortisol

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75
Q

Mineralocorticoids = ________________

A

Aldosterone

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76
Q

What are the spinal effects of opioids?

A

Inhibitory effect is mediated
by opioid receptors that are
located on both presynaptic
and postsynaptic membranes
of pain-mediating synapses…

Decreased transmitter release from presynaptic neuron…

Decreased excitability (hyperpolarization) of postsynaptic neuron…

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77
Q

What are the supraspinal (brain) effects of opioids?

A

1) Opioids bind to specific receptors in the midbrain periaqueductal gray matter (PAG) and remove inhibition (disinhibition) of descending pathways that decrease pain.

2) Increased activity of descending pathways travels through the ventromedial medulla (VMM) to reach the dorsal horn of the spinal cord.

3) Neurons in descending pathways release serotonin and norepinephrine onto dorsal horn synapses and inhibit the ability of these synapses to transmit painful impulses to the brain.

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78
Q

What are the peripheral effects of opioids?

A

Opioids decrease excitability of the neuron (nociceptor) and inhibit the neuron from initiating transmission of
painful stimuli toward the spinal cord

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79
Q

When are opioids typically used?

A

1) after surgery
2) after trauma
3) after myocardial infarction
4) during chronic pain, like cancer

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79
Q

What are the mechanisms for tolerance?

A

▪ Receptor down-regulation (removed by endocytosis) and desensitization.

▪ Loss of communication between the opioid receptor and the G protein.

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80
Q

What are some other opioid uses?

A

➢ Anesthetic pre-medication or as an adjunct in general anesthesia.

➢ Cough suppression (short-term use of codeine and codeine-like agents).

➢ Control of severe diarrhea.

➢ Acute pulmonary edema.

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80
Q

Withdrawal symptoms become evident
within ____________ after the last dose of
the drug, and peak on _____________
after the drug has been stopped; last
about ____________

A

6 to 10 hours — day 2 or day 3 — 5 days

81
Q

Tolerance begins after the ___________ of the narcotic, but the need for increased amounts of the drug usually becomes obvious after ____________ of administration.

A

first dose — 2 to 3 weeks

82
Q

Tolerance seems to last approximately _____________ after the drug is removed.

A

1 to 2 weeks

83
Q

Glucocorticoids act on __________________ in order to ___________________.

A
  • macrophages, lymphocytes, and endothelial cells
  • inhibit the expression of inflammatory proteins (cytokines)
84
Q

What are the applications of glucocorticoids?

A

1) decrease inflammation

2) immunosuppression

3) replacement steroid for adrenal insufficiency

85
Q

What are the pharmacological properties of NSAIDs? (What are they for?)

A

► To decrease inflammation.
► To relieve mild-to-moderate pain (analgesia).
► To decrease elevated body temperature associated with fever (antipyresis).
► To decrease blood clotting by inhibiting platelet aggregation (anticoagulation).

86
Q

What are the 3 eicosanoids?

A

1) LT = leukotriene
2) PG = prostaglandin
3) TX = thromboxane

87
Q

COX-1 vs. COX-2

A
  • COX-1 enzyme is a “normal” cell component that synthesizes PG to help regulate and maintain cell activity. (Not always beneficial)
  • COX-2 often represents an “emergency” enzyme that synthesizes PG in response to cell injury. (i.e., pain and inflammation) (Not always harmful)
88
Q

What does aspirin do?

A
  • Alleviates pain and inflammation, decreases fever, and affects blood clotting.
89
Q

What are the clinical applications of aspirin-like drugs?

A
  1. Pain and Inflammation
  2. Fever
  3. Vascular Disorders
  4. Prevention of Cancer
90
Q

What are some problems and adverse effects of aspirin-like drugs?

A
  1. Gastrointestinal Problems - (loss of protective prostaglandins from the mucosal lining)
  2. Cardiovascular Problems - (increase blood pressure and the chance of thrombotic events via inhibition of PGE2 and PGI2, which are vasodilators)
  3. Other Side Effects - (adverse changes in hepatic function and renal failure)
91
Q

What are some strategies to manage GI problems produced by aspirin-like drugs?

A

➢ Enteric-coated aspirin tablets (pros and cons)

➢ Taking with meals (pros and cons)

➢ Use of other drugs in conjunction
▪ Proton pump inhibitors, histamine receptor (H2) blockers, COX-2 selective drugs

92
Q

What are the different types of hyperparathyroidism?

A

 Primary
▪ One or more of the parathyroid glands enlarge (hyperplasia or adenoma).
▪ Normal regulatory relationship between serum calcium levels and PTH secretion is interrupted.

 Secondary
▪ Glands are hyperplastic from malfunction of another organ system.
▪ Compensatory response to chronic hypocalcemia due to renal failure (decreased renal
activation of vitamin D) or others.

 Tertiary
▪ Exclusively in dialysis clients who have long-standing secondary hyperparathyroidism.
▪ Glands ultimately become autonomous in function and unresponsive to serum calcium levels.

93
Q

Excessive circulating PTH leads to ________________________________.

A

bone damage, hypercalcemia, and kidney damage

94
Q

How would you treat primary hyperparathyroidism?

A

surgical removal (parathyroidectomy)

95
Q

Disorders of the parathyroid glands can cause _____________________.

A

periarthritis and tendinitis

96
Q

What is the most common cause of hypoparathyroidism?

A

Iatrogenic = glandular damage or accidental removal during thyroid removal or anterior neck surgery

97
Q

Epinephrine and norepinephrine exert widespread effects on _______________________________ and affect _______________________________.

A
  • vascular tone, the heart, the nervous system
  • glucose metabolism
98
Q

Epinephrine = _____________

A

adrenaline

99
Q

What are some disorders of the adrenal glands?

A
  1. Primary Adrenal Insufficiency (Addison Disease)&raquo_space;> insufficient cortisol release AND aldosterone release
  2. Secondary Adrenal Insufficiency&raquo_space;> insufficient cortisol release only
  3. Adrenocortical Hyperfunction
    ➢ Cushing Syndrome&raquo_space;> glucocorticoid (cortisol) excess
    ➢ Conn Syndrome&raquo_space;> aldosterone excess
100
Q

What are the clinical manifestations of Addison Disease?

A

1) Decreased production of cortisol (a glucocorticoid)
▪ Gluconeogenesis decreases, with resultant hypoglycemia and liver
glycogen deficiency.
▪ Grows weak, exhausted, hypotensive, and suffers from anorexia, weight loss, nausea, and vomiting.
▪ Diminishes resistance to stress.

2) Chronic cortisol deficiency results in a failure to inhibit anterior pituitary secretion of ACTH. (it taps out)
▪ The result is a simultaneous increase in ACTH secretion and melanocyte-stimulating hormone (MSH).
▪ Excessive MSH increases skin and mucous membrane pigmentation (a bronzed or tanned appearance).

3) Aldosterone (a mineralocorticoid) deficiency
▪ Causes numerous fluid and electrolyte imbalances.
▪ Increased sodium excretion, dehydration, hypotension (low blood pressure causing orthostatic symptoms), and decreased cardiac output affecting heart size (decrease in size).
▪ Eventually, hypotension becomes severe and cardiovascular activity weakens, leading to circulatory collapse, shock, and death.

101
Q

____________________ are the hallmark of Addison disease.

A

Decreased serum cortisol levels

102
Q

What is “addisonian crisis”?

A

the body is unable to meet the cortisol demand caused by the extra “stress” of exercise

103
Q

It is most likely to see _____________ adrenal insufficiency as a result of ______________________.

A
  • secondary
  • suppression of ACTH
104
Q

Symptoms of secondary adrenal insufficiency are related to _________________ only.

A

cortisol deficiency

105
Q

What is the treatment for secondary adrenal insufficiency?

A

replacement of ACTH

(b/c aldosterone is still fine…cortisol deficiency is apparent b/c of lack of ACTH)

106
Q

Cushing Syndrome (hypercortisolism) is a result of _______________________.

A

1) hyperfunction of the adrenal gland (usually benign or malignant adenomas, rarely a carcinoma)&raquo_space;> CUSHING SYNDROME

2) an excess of corticosteroid medication

3) an excess of ACTH stimulation from the pituitary gland (or other sites)&raquo_space;> CUSHING DISEASE

107
Q

Cortisol has a key role in ______________ and a lesser part in ________________________.

A
  • glucose metabolism
  • protein, carbohydrate, and fat metabolism
108
Q

________________ occurs when conditions such as ____________________________________ cause changes like those of Cushing syndrome.

A
  • Pseudo-Cushing syndrome
  • depression, alcoholism,
    estrogen therapy, or eating disorders
109
Q

What are the clinical manifestations of Cushing Syndrome?

A

1) hyperglycemia
2) hypertension
3) proximal muscle wasting
4) osteoporosis
5) weakening of protein structures

110
Q

What lab studies would you use to diagnose Cushing Syndrome?

A

urine and serum cortisol

111
Q

Therapists are more likely to treat people who have developed ________________ Cushing syndrome.

A

medication-induced (exogenous steroid administration)

112
Q

Conn Syndrome = ________________

A

primary aldosteronism

113
Q

An adrenal lesion results in hypersecretion of aldosterone, known as _________________.

A

Conn Syndrome

114
Q

An excess of _____________ enhances __________________ by
the kidneys.

A
  • aldosterone
  • sodium reabsorption
115
Q

_____________________ is the largest endocrine organ in the body because _________________________.

A
  • Adipose tissue
  • secretes several hormones responsible for metabolism, hunger, vasoconstriction, and cellular growth and development
116
Q

What do adipokines do?

A

Maintain the balance of energy by regulating appetite, energy
expenditure, insulin sensitivity, and lipid uptake.

(They come from adipose tissue.)

117
Q

The amount of ____________ fat decreases into adulthood.

A

brown

118
Q

Brown fat is a specialized tissue that is important in ______________________________.

A

thermoregulation (converting energy from food into heat)

119
Q

______________ is the classic adipose tissue responsible for ____________________.

A
  • white fat
  • storage of triglycerols (to provide a long-term reservoir of energy for the body)
120
Q

Fat accumulated in the __________________ results in a pear-shaped figure.

Fat accumulated in the __________________ results in a apple-shaped figure.

A
  • lower body (subcutaneous fat)
  • abdominal area (visceral fat)
121
Q

“Keep your _______________________ to less than _______________________.”

A
  • waist circumference
  • half your height
122
Q

Obesity is a multifactorial disease with complex interactions between _____________________________.

A

lifestyle, environment, and genetics

123
Q

Viral infections (infectoobesity)&raquo_space;> ____________________

A

Adenovirus-36 (Ad-36)

124
Q

Hormonal dysfunction in obesity&raquo_space;> _____________________

A

Affects the hypothalamic-pituitary-adrenal (HPA) axis

125
Q

What are treatments for obesity?

A

▪ Weight loss
▪ Medications
▪ Surgery (bariatric)
▪ Behavioral and lifestyle changes

126
Q

Islets constitute ____________ of
pancreas.

A

1%~2%

127
Q

Diabetes disrupts the metabolism of __________________________.

A

carbohydrates, fats, and proteins

128
Q

Type 1 Diabetes = ___________

A

insulin deficiency (body doesn’t make enough insulin)&raquo_space;> 5-10%

129
Q

Type 2 Diabetes = ___________

A

insulin resistance (body can’t use insulin properly)&raquo_space;> 90-95%

130
Q

Diabesity is considered an _________________________.

A

inflammatory metabolic condition

131
Q

Gestational diabetes is any degree of glucose intolerance recognized with the onset of pregnancy (_____________ of gestation)

A

24-28 weeks

132
Q

What occurs when the body cannot utilize glucose the way it should?

A

prediabetes (precursor to type 2 diabetes)

133
Q

A1c is a person’s average blood sugar level for the previous ______________________.

A

3 months

134
Q

1 in every ______ people __________________.

1 in every ______ people __________________.

More than 1 in ______ people _____________________.

More than _____ in 10 people _____________________.

A
  • 10 … have diabetes
  • 5 … don’t know they have diabetes
  • 3 … have prediabetes
  • 8 … don’t know they have prediabetes
135
Q

Type 2 diabetes –> insulin resistance –> _____________________

A

β cells stress –> decrease β cells mass

136
Q

What are the macrovascular damages of hyperglycemia?

A

Affects arteries that supply the heart, brain, and lower extremities

137
Q

What are the microvascular damages of hyperglycemia?

A

Affects retina, renal glomerulus, and peripheral nerve

138
Q

Diabetic Ketoacidosis (DKA) is most commonly seen in _________________.

A

Type 1 Diabetes

139
Q

Diabetic Ketoacidosis (DKA) is characterized by the triad of
_____________________________.

A

hyperglycemia, acidosis, and
ketosis

**the body can’t use the glucose, so it uses fat instead (ketosis), which in turn causes acidosis (acid levels rise b/c of the breakdown of fat)

140
Q

What are the classic symptoms of type 2 diabetes?

A

polyuria (frequent urination) and polydipsia (frequent thirst)

141
Q

What are the glycemic recommendations for non-pregnant adults with diabetes?

A
  • A1c < 7.0%
  • Preprandial capillary plasma glucose = 80–130 mg/dL
  • Peak postprandial capillary plasma glucose <180 mg/dL
142
Q

How should you manage your diabetes?

A

medications, stay active, eat healthy

143
Q

About ___________________ and ______________________ are attributable to diabetes.

A
  • 50% of myocardial infarctions
  • 75% of strokes
144
Q

_______________ raises a person’s risk of dying from heart disease by ________________.

A
  • type 2 diabetes
  • 2 to 3 times
145
Q

The upper GI tract includes the _____________________________.

A

mouth, esophagus, stomach, and duodenum

146
Q

The lower GI tract includes the _____________________________.

A

small and large intestine

147
Q

The upper GI tract aids in ___________________________.

A

the ingestion and digestion of food

148
Q

The small intestine aids in ___________________________.

A

digestion and absorption of nutrients

149
Q

The large intestine aids in ___________________________.

A

absorbs water and electrolytes, storing waste products of digestion until elimination

150
Q

___________________ has ______________ of the body’s immune cells.

A
  • Gut immune system
  • 70% to 80%
151
Q

Changes within the alimentary tract include decreases in ______________________________.

A

1) gastric motility
2) blood flow
3) nutrient absorption
4) volume and acid content of gastric juice

152
Q

What is a hiatal hernia?

A

Esophageal hiatus of the diaphragm becomes enlarged, allowing the stomach to pass through the diaphragm into the thoracic cavity.

153
Q

What are some risk factors of hiatal hernia?

A

Factors that weaken the diaphragm muscle or alter the hiatus and increases intraabdominal pressure.

154
Q

What are some symptoms of hiatal hernia?

A

heartburn (remember: HHH) and reflux

155
Q

If a hiatal hernia is present, what should you avoid?

A

Avoid flat supine position and any exercises requiring the Valsalva maneuver (which increases intraabdominal pressure)

156
Q

What is GERD (Gastroesophageal Reflux Disease)?

A

The consequences from the reflux backward flow) of gastric contents into the esophagus accompanied by a failure of anatomic and physiologic mechanisms to protect the esophagus. (Can be erosive or non-erosive.)

157
Q

What are the 3 factors that keep the esophagus healthy?

A
  1. Anatomic barriers between the stomach and the esophagus.
  2. Mechanisms to clear the esophagus of stomach acid.
  3. Maintaining stomach acidity and acid volume.
158
Q

What is an esophageal manifestation of GERD?

A

heartburn (just like hiatal hernia)

159
Q

When it comes to GERD, adults _____________ are more likely to have ___________________.

A
  • > 70 y/o
  • atypical symptoms
160
Q

What are the extra-esophageal manifestations of GERD?

A

Asthma, cough, and laryngitis

161
Q

What are some lifestyle modifications for GERD?

A

1) avoid aggravating foods
2) smoking cessation
3) reduce alcohol consumption
4) reduce caffeine consumption
5) weight loss
6) elevation of the bed

162
Q

What are the medications for GERD?

A

Nonprescription antacids, H2 blockers, and proton pump inhibitors (PPIs)

163
Q

What is PUD (Peptic Ulcer Disease)?

A

A break in the lining of the stomach or
duodenum of 5 mm or more owing to a
number of different causes.

164
Q

What exogenous substances can cause PUD?

A

NSAIDs, low-dose aspirin, and H. pylori bacterial infection (most common causes - 90%)

165
Q

What are the mucosal defenses?

A

Mucous and bicarbonate layer, an epithelial barrier, prostaglandins, and adequate mucosal blood flow.

166
Q

What are the mucosal “insults”?

A

Acid, pepsin, alcohol, bile salts, and drugs.

167
Q

The classic symptom of PUD, when present, is _______________________.

A

epigastric pain described as burning, gnawing, or cramping near the xiphoid or radiating to the back

(pain may be relieved with eating or occur at night)

168
Q

What are some complications that come with PUD?

A

1) Bleeding (acute and chronic)
▪ Hematemesis (vomiting blood)
▪ Hematochezia (bleeding per rectum)
▪ Coffee-ground emesis
▪ Melena (dark, tarry stools secondary to blood)

2) Perforation
▪ Sudden severe pain (thoracic spine from T6 to T10 with
radiation to the right upper quadrant)

3) Penetration
▪ Ulcer erodes into adjacent organs (small bowel, pancreas, or liver)

4) Gastric outlet obstruction

169
Q

What is hematemesis?

A

vomiting blood

170
Q

What is hematochezia?

A

bleeding per rectum

171
Q

What is melena?

A

dark, tarry stools secondary to blood

172
Q

What is gastric outlet obstruction?

A

opening between the stomach and the small intestine (specifically the duodenum) becomes blocked, preventing the normal passage of food and liquids from the stomach into the intestines

173
Q
  • Referred pain patterns:

▪ Perforations and hemorrhage cause ______________.

▪ Ulcer pain radiates to the _______________ and ________________.

A
  • back pain
  • mid-thoracic back, right shoulder pain
174
Q

What is inflammatory bowel disease (IBD)?

A

A polygenic disease with complex interactions between gut microbiota, host immunity, and intestinal mucosal response.

175
Q

What are the 2 forms of inflammatory bowel disease (IBD)?

A

 Crohn Disease (CD)

 Ulcerative Colitis (UC)

176
Q

What is Crohn Disease?

A

A chronic, lifelong inflammatory disorder that can affect any segment of the intestinal tract, although most commonly it affects the ileum and/or colon.

177
Q

What is Ulcerative Colitis?

A

A chronic inflammatory disorder of the mucosa of the colon, typically involving the rectum, which can then advance proximally in a continuous manner to involve the entire colon.

178
Q

What are some extra-intestinal manifestations of inflammatory bowel disease (IBD)?

A
  • Joint involvement ranging from arthralgia to acute arthritis (most common)
  • Arthropathies (peripheral and axial)
179
Q

What is the referred pain for inflammatory bowel disease (IBD)?

A

Periumbilical pain (low back and lower
right quadrant)

180
Q

What is diverticulosis?

A

▪ The presence of outpouchings (diverticula) in the wall of the colon or
small intestine.

▪ The mucosa and submucosa herniate through the muscular layers of the
colon to form outpouchings

181
Q

What is diverticulitis?

A

▪ Inflammation/infection of the diverticula with possible complications
such as perforation, abscess formation, obstruction, fistula formation,
and bleeding.

182
Q

Diverticular disease is ______________ in ______ of affected people.

A

asymptomatic – 80%

183
Q

Diverticular disease - uncomplicated:

A

▪ Mild symptoms: nonspecific and episodic pain (may overlap with
symptoms of IBS)

▪ When diverticula become blocked, bacteria that are trapped inside
begin to proliferate, causing infection and inflammation

184
Q

Diverticular disease - complicated:

A

▪ A fistula (abnormal connection or passageway between two organs) may develop with the bladder (colovesical fistula)

▪ Pneumaturia (air in the urine), fecaluria (urine in the stool), or
recurrent urinary tract infections, in conjunction with fever, abdominal
pain, or palpable mass

185
Q

In diverticular disease, a CT scan will show ________________.

A

elevated WBC’s

186
Q

In diverticular disease, prognosis is __________.

There is ___________ mortality for diverticulitis.

A
  • good
  • low
187
Q

What is appendicitis?

A
  • An inflammation of the vermiform
    appendix that often results in
    necrosis and perforation with
    subsequent localized or generalized
    peritonitis.
188
Q

Peak incidence of appendicitis is between the ages of ________________. More common in _______________.

A
  • 15 and 19
  • males
189
Q

Appendicitis is primarily from ___________________________ and secondarily from _______________________. One-third are caused by __________________________.

A
  • obstruction of the lumen
  • bacterial infection
  • obstruction that prevents normal drainage
190
Q

What are the clinical manifestations of appendicitis?

A

Abdominal (epigastric, periumbilical, or right lower quadrant) pain accompanied by anorexia, nausea, vomiting, and low-grade fever in adults (high fevers if perforation)

191
Q

In appendicitis, there is point tenderness over the site at _______________________.

A

McBurney point

192
Q

In appendicitis, WBC’s will be ________________.

A

> 20,000/mm3

193
Q

_______________ of appendicitis cases are ______________ because of the __________________________________.

A
  • 40% to 50%
  • atypical
  • position of the tip of the appendix (not in right lower quadrant)
194
Q

What are the treatments for appendicitis?

A

▪ Antibiotics OR…

▪ Appendectomy, or surgical removal,
is performed ASAP, either by open
procedure or laparoscopically (for
uncomplicated patients)

195
Q

Client with appendicitis may present with symptoms of ___________________.

A

right thigh pain, groin (testicular) pain, pelvic pain, or referred pain in the hip

196
Q

What is a rectal fissure?

A

A rectal or anal fissure is an ulceration or tear of the lining of the anal canal, usually on the posterior wall.

197
Q

What is an acute fissure?

A

An acute fissure occurs as a result of excessive tissue stretching or tearing, such as childbirth or passage of a large, hard bowel movement through the area.

198
Q

Anal fissures frequently heal within ___________________ when treated with _______________________________________.

A
  • 1-2 months
  • a combination of bran and bulk laxatives or stool softeners, sitz baths, and emollient suppositories
199
Q

What are hemorrhoids?

A

Hemorrhoids, or piles, are varicose
veins of a pillow-like cluster of veins
that lie just beneath the mucous
membranes lining the lowest part of
the rectum and anus.

200
Q

Hemorrhoids are associated
especially with anything that
__________________________.

A

increases intraabdominal pressure (similar to hiatal hernia)

201
Q

Internal VS. External hemorrhoids:

A

 Internal hemorrhoids
▪ Occur in the lower rectum and usually are noticed first when a small amount of
bleeding occurs during passage of stool, especially if straining occurs during a
bowel movement.

 External hemorrhoids
▪ Located under the skin around the anus bleed (bright red blood) if the
hemorrhoid is injured or ulcerated and are very painful because they form in
nerve-rich tissue outside the anal canal.
▪ It can be treated with a local application of topical medications, sitz baths, high
fiber diet, and avoidance of constipation and other causes of increased
intraabdominal pressure

Internal Medicine - EXAM 3 (2 decks)

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