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Professional Development > Part 26 > Flashcards

Part 26 Flashcards

1
Q

Blood calcium levels range to determine treatment

A
  • Asymptomatic or mildy symptomatic <12mg/dL does not require immediate treatment
  • 12-14mg/dL may be tolerated well if chronic but not if acute
  • > 14mg/dL requires urgent treatment regardless of symptoms
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2
Q

Hypercalcemia treatment (4)

A
  • Isotonic saline to correct for volume depletion and vomiting
  • Exogenous salmon calcitonin for rapid short term treatment but wears off (tachyphylaxis)
  • Biphosphonates (takes a few days to activate but eventually take over from the calcitonin)
  • Calcimimetics such as cincalcet in patients in parathyroid dz
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3
Q

3 types of hyponatremia and common causes

A

Hypovolemia - GI losses, renal losses from thiazide diuretics
Euvolemia - SIADH, primary polydipsia
Hypervolemia - heart failure, cirrhosis

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4
Q

Most common endocrine disorder of women and most common cause of infertility

A

PCOS

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5
Q

PCOS pathophysiology

A

Hypothalamic pituitary abnormalities resulting in altered LH action increasing the LH:FSH ratio >2 and increased sensitivity to androgens (hyperandrogenism) including androstenedione, DHEA-S, and testosterone, and also see insulin resistance (50-70% are hyperinsulinemic and at risk for pre-diabetes and overt type 2 diabetes

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6
Q

PCOS and insulin

A

Due to genetic and environmental factors, ovaries and thecal cells in ovaries that make estrogen and a little bit of testosterone are very sensitive to higher insulin levels and insulin serves as a co-gonadotropin so that instead of LH stimulating these cells insulin does instead to see increased androgen production by the ovaries

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7
Q

High risk groups for PCOS (4)

A
  • oligo-ovulatory infertility
  • obesity and insulin resistance
  • diabetes type 2 (typically)
  • family members with pcos
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8
Q

PCOS presenting signs/symptoms (9)

A
  • Secondary amenorrhea (rule out pregnancy)
  • other menstrual irregularities
  • androgen excess (hirsutism, acne, male pattern baldness)
  • obesity
  • cystic ovaries (usual but not diagnostic)
  • glucose intolerance
  • metabolic syndrome
  • Nonalcoholic steatohepatitis (NASH) (very common cause of cirrhosis in US)
  • miscarriage risk
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9
Q

PCOS diagnostic criteria NIH (3)

A
  • Menstrual irregularity
  • clinical or biochemical evidence of hyperandrogenism
  • ruling out other causes of menstrual irregularity
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10
Q

PCOS diagnostic criteria Rotterdam

A

2 of the following

  • Evidence of androgen excess
  • Ovulatory dysfunction
  • polycystic ovaries
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11
Q

Most sensitive test for hyperandrogenism in PCOS eval

A

Free testosterone first thing in morning

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12
Q

Look for other causes than PCOS when you have these 3 things

A
  • Sudden onset or worsening of symptoms
  • onset 3rd decade of life or later
  • signs of virilization (frontal balding, severe acne, clitoromegaly, muscle mass, deepening voice)
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13
Q

Test to rule out acquired congenital adrenal hyperplasia in a suspected PCOS patient

A

Test for 17 hydroxyprogesterone elevation

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14
Q

PCOS therapeutic options (6)

A
  • Birth control pills to lower free testosterone (Yaz)
  • Antiandrogens (spironolactone)
  • Metformin
  • weight loss
  • clomiphene (80% ovulate in response to this allowing almost 50% to conceive)
  • bariatric surgery (curative)
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15
Q

First trimester, third trimester, adolescence, and adult consequences of impaired testosterone secretion

A

1st trimester - female external genitalia, partial virilization
3rd trimester - micropenis
Adolescence - incomplete puberty
Adult - energy, libido, decreased hair, loss of muscle mass, severe osteoporosis

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16
Q

Kallmann’s syndrome

A

Male individuals who have lifelong hypogonadism and also have anosmia due to deficient secretion of GnRH

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17
Q

Klinefelter’s syndrome

A

Genetic abnormality of two x chromosomes on a male patient resulting in infertility and hypogonadism

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18
Q

Eunuchoid proportions

A

Measured when floor to pubis are measured as 2cm longer than pubis to crown of a patient indicative of male hypogonadism

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19
Q

Lab tests for male hypogonadism (4)

A
  • Serum total testosterone (most important test avoid when hospitalized or on steroid therapy)
  • LH and FSH
  • serum free testosterone (binding protein abnormality suspected)
  • Prolactin levels
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20
Q

Diurnal fluctuation of testosterone

A

Highest in the morning, lowest in the evening

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21
Q

Primary hypogonadism causes (4)

A
  • Congenital abnormalities such as klinefelters
  • Bilateral cryptorchidism (undescended testes)
  • varicocele
  • Infection such as mumps
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22
Q

Secondary hypogonadism causes (4)

A
  • Kallmann’s syndrome (deficient secretion of GnRH)
  • isolated hypogonadotropic hypogonadism
  • systemic illness and long term steroid treatments
  • chronic opiate administration
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23
Q

Issue with oral preparations of testosterone

A

Almost impossible to maintain normal levels with them, also liver toxic due to first pass effect

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24
Q

Male hypogonadism testosterone treatment options (2)

A
  • Injectable Tetosterone 100mg weekly or 300 every 3 weeks (fluctuations occur)
  • transdermal patch or gel
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25
Q

Undesirable effects of testosterone treatment (5)

A
  • acne
  • gynecomastia over first few months (body converts to estrogen initially)
  • physically aggressive behavior
  • PSA level increases but should remain in normal range (BPH isn’t a problem)
  • 2ndary polycythemia vera
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26
Q

Gynecomastia pathogenesis

A
  • Decreased androgen production

- Increased estrogen production

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27
Q

Testosterone variation with age

A

100 ng/dl DECREASE from age 20-80 especially in free testosterone, will see symptoms comparable to hypogonadism

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28
Q

Type 1.5 diabetes

A

Adult onset that appears initially like type 2 diabetics but are usually healthy, fit, and thin and then over time progresses into type 1 diabetes

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29
Q

For sliding scale insulin dosing, 1 unit acting insulin corresponds to ingestion of ___ g of carb

A

12-15

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30
Q

Thyroid hormone mech of action

A
  • T3, the only active form enters the cell and binds specific receptors located in the cell’s nucleus
  • induces transcription of specific DNA segments which ultimately results in altered protein synthesis in the cell
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31
Q

Plummer’s disease/toxic nodular goiter

A

Recult of thyroid adenoma that clinical manifestts similar to graves disease but without exopthalmos, requires surgery and radiation

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32
Q

Desiccated thyroid (Thyroid USP/armour thyroid)

A

Obsolete treatment for hypothyroidism only still used in those who have been on it for years derived from porcine, has higher T3:T4 ratio which can lead to fluctuating levels of T3

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33
Q

Propylthiouracil (PTU) function and ADR’s (3)

A
  • Used alone as sole source of treatment in graves disease or employed as adjunct to radiation therapy
  • Agranulocytosis, hypothyroidism, liver injury (sudden onset)
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34
Q

Potassium iodide (thyro-block)

A

PO to protect thyroid in event of radiation emergency (such as a nuclear accident) that prevents uptake of radioactive iodide preventing harm to thyroid gland

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35
Q

Radioactive iodine 131 I

A

Radioactive isotope of stable iodine to produce clinical remission in hyperthyroid patients by destroying the gland without damaging surrounding tissue

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36
Q

Aldosterone physiologic effects

A

Acts on the collecting ducts of nephron to promote Na+ resorption in exchange for K+ or H+ excretion (without it see hyponatremia and hyperkalemia, and acidosis), regulated by angiotensin II not ACTH

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37
Q

Adrenal adenoma and carcinoma causing hypersecretion of glucocorticoids is cushings….

A

….syndrome

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38
Q

Hypersecretion of ACTH by pituitary adenomas resulting in excess glucocorticoids is cushings…

A

….disease

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39
Q

Primary hyperaldosteronism results in these 3 things and can be treated with what drug?

A
  • Causes hypokalemia, metabolic alkalosis, and hypertension
  • Aldosterone antagonist spironolactone
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40
Q

Secondary and tertiary adrenocortical insufficiency does not effect ____ because…

A

mineralcorticoid secretion
….they are managed by the angiotensin II aldosterone system!

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41
Q

Adrenal crisis

A

Hypotension, dehydration, weakness, lethargy, and GI symptoms that can progress into shock and death caused by adrenal failure, pituitary failure, or failure to replace/sudden withdrawal from glucocorticoid therapy

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42
Q

Fludrocortisone function and ADR’s (3)

A

Only mineralocorticoid available to mimic the body’s natural conc. and used for chronic replacement
-Excessive salt and h2o retention, cardomegaly, hypokalemia

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43
Q

Drug of choice for chronic adrenal insufficiency

A

Cortisone and hydrocortisone

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44
Q

Whipple’s triad and what is it pathognomonic for

A
  • Fasting hypoglycemia symptoms
  • Serum glucose <50
  • symptoms improve with sugar

Insulinoma presence

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45
Q

Honeymoon phenomenon type 1 diabetes

A

Period shortly after type 1 diabetes diagnosis in which not very large dosages of insulin are needed to treat because the pancreas is still making its own to an extent, does not occur in all patients and is temporary but can be prolonged with certain lifestyle modifications

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46
Q

The dawn effect

A

Abnormal high early morning (2-8am) early morning glucose in patients with diabetes

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47
Q

The somogyi effect

A

high blood sugar in AM as a response to rebound low blood sugar at night

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48
Q

Metabolic syndrome diagnostic criteria

A

3 or more of the 5 following

  • waist circumference >35in in women and >40 in men
  • triglycerides >150
  • Low HDL <50
  • High BP > 135/85
  • fasting glucose >110
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49
Q

Pemberton sign

A

Test for venous obstruction due to a goiter, positive when bilateral arm elevation causes facial erythema and cyanosis compressing the thoracic inlet indicating goiter presence

50
Q

The right adrenal gland’s main vein (right suprarenal vein) drains directly into the ___, the left drains ___

A
  • vena cava

- renal vein

51
Q

Layers of the adrenal gland and hormones secreted in each (4)

A

Zona Glomerulosa - aldosterone
Zona fasciculata - cortisol
Zona reticularis - androgens
Medulla - catecholamines

52
Q

4 common extramedullary locations of pheochromocytoma (catecholamine secreting paragangliomas that only secrete norepi)

A
  • Organ of Zuckerkandl (near bifurcation of abdominal aorta along spine)
  • neck
  • upper abdomen (most common)
  • bladder
53
Q

Classic triad of pheochromocytoma and another pathognomonic finding

A
  • palpitations
  • sweating
  • headache

-feeling of impending doom

54
Q

Pheochromocytoma treatment options (1) and what is the pre op prep?

A
  • surgical resection only (dissection with minimal tumor manipulation to prevent catecholamine surge, venous drainage first*** then arterial)
  • Pre op prep involving preventing hypertension and tachycardia beginning 1 week before (alpha adrenergic antagonist like phenoxybenzamine THEN B receptor antagonist like propranolol
55
Q

Aldosteronoma pathognomonic findings (2)

A
  • hypertension
  • hypokalemia (not on diuretics)
56
Q

Recall the RAAS system

A
  • at the level of the kidneys hypovolemia causes release of renin from juxtaglomerular aparatus
  • angiotensinogen released from liver is converted by renin to angiotensin I
  • angiotensin I is converted by lungs that release ACE into angiotensin II
  • angiotensin II causes aldosterone secretion at the adrenal gland and has peripheral vasoconstriction effects
  • aldosterone causes retention of sodium and therefore water but loss of potassium
57
Q

Diagnostic labs of aldosteronoma (4)

A
  • increased plasma aldosterone but decreased plasma renin (inappropriate release of aldosterone)
  • rule out bilateral adrenal hyperplasia (unknown cause) via CT scan
  • oral sodium loading (should suppress aldosterone secretion)
  • captopril administration test (should cause decrease in adlosterone and increased renin but in primary hyperaldosteronism there is no change)
58
Q

Cushing syndrome vs cushing dz

A

Syndrome is signs and symptoms associated with elevated cortisol level vs in cushing dz see pituitary tumor hypersecreting ACTH resulting in excess cortisol

59
Q

Glucocorticoid producing tumor diagnostic studies (3)

A
  • increased 24 hr urine free cortisol
  • dexamethasone suppression test
  • CT scan
60
Q

Cushing syndrome signs and symptoms (8)

A
  • weight gain
  • peripheral muscle wasting
  • hirsutism
  • buffalo hump
  • moon face
  • menstrual irregularity
  • amenorrhea
  • impotence
61
Q

Cortisol release pathway

A
  • cortosol levels sensed in hypothalamus and releases CRH when low
  • Anterior pituitary receives CRH and this stimulates release of ACTH
  • this acts at the adrenal gland increasing cortisol in the blood stream to be sensed in hypothalamus
62
Q

Cushings disease has __ ACTH and ___ cortisol, noncushings disease cushings syndrome has ___ ACTH and ___ cortisol

A

Elevated, elevated, low, elevated

63
Q

Dexamethasone suppression test

A

-24 hr urine for 3 consecutive days, .5 mg of dexamethasone given every 6 hours on day 2 and 3, urinary free cortisol should be <10mcg/day on day 2, if not suppressed then must have adenoma

64
Q

Adrenal cortex incidentaloma

A

Seen in patients often getting CT or screening for something else, if it isn’t presenting symptomatic then don’t need surgical intervention, can do fine needle aspiration after ruling out a pheo*** to determine cause

65
Q

Most common functional pancreatic endocrine tumor

A

Insulinoma

66
Q

Diagnosis of insulinoma (3)

A
  • insulin and glucose determinations during a 72 hr fast
  • insulin to glucose ration >.3 after overnight fast
  • elevated c peptide and proinsulin levels
67
Q

Proinsulin is cleaved to insulin from removal of a free ___, measuring this rules out ___ insulin as a source

A

C peptide, exogenously injected

68
Q

Zollinger Ellison syndrome/gastrinoma suspicious findings (5)

A
  • ulcers in unusual locations (not antrum or prepyloric area)
  • persistent ulcers despite medical management and chronic diarrhea
  • ulcers and manifestations of other endocrine tumors
  • strong family history of ulcer dz
  • recurrent ulcers after antiulcer surgery
69
Q

Gastrinoma diagnostic studies (2)

A
  • fasting gastrin >200 or >1000 highly suspicious
  • secretin stimulation increasing gastrin levels >200 is diagnostic***
70
Q

Gastrinoma treatment options (2)

A
  • control gastric hypersecretion (gastrin, Ach from vagus, histamine all contributors) so give PPI
  • surgical localization, assess for mets, and remove
71
Q

Pyramidal lobe of the thyroid

A

Remnant of thyroglossal duct sometimes present extends upward torward cricoid cartilage from isthmus

72
Q

Thyroid arterial supply (3)***

A
  • Inferior thyroid artery from the thyrocervical trunk
  • Superior thyroid artery off carotid
    -rarely thyroid ima artery
73
Q

Thyroid venous supply (3)***

A
  • Inferior thyroid vein draining into subclavian
  • middle thyroid vein (has NO arterial equivalent)
  • superior thyroid vein draining into jugular
74
Q

Hemopoiesis definition

A

Production of formed elements of blood (erythrocytes, leukocytes, thrombocytes)

75
Q

Red marrow location in children vs adults

A

Nearly all marrow in children is red, in adults it is confined to specific areas (skull, ribs and sternum, pelvis primarily) of bone, with yellow marrow replacing it in other locations (although it can convert back)

76
Q

Hemocytoblast

A

Stem cells that form all elements of blood, also known as a pluripotential stem cell

77
Q

Differentiation of stem cells occurs when they develop surface receptors for a specific 1 of 3 of these growth factor’s in which they are then committed for life to that line

A
  • erythropoietin (transforms an uncommitted potential cell to a committed proerythroblast)
  • thrombopoietin
  • CSF’s
78
Q

Erythrocyte differentiation pathway (5)

A 
Hemocytoblast
Proerythroblast
Erythroblast
Reticulocyte (enters circulation) 
mature RBC
79
Q

Erythrocyte homeostasis mechanism of action

A
  • Drop in O2 content detected by receptors in kidney
  • increases output of erythropietin by kidneys
  • 3-4 days later, RBC rises and compensates for dropped O2 content
80
Q

Major requirements for erythropoiesis to occur and what function do they serve(2)

A
  • Iron (form hemoglobin)
    • B12 and folic acid (proper cell division)
81
Q

Iron metabolism and storage in the liver mechanism of action pathway

A
  • Fe3+ is converted to Fe2+, or ingested Fe2+ sits in the gut
  • Only Fe2+ can be absorbed by small intestine binding gastroferrin produced by stomach
  • Dissociates from gastroferrin and binds transferrin to deliver to tissues of the body
  • liver binds any excess iron to apoferrin, the iron storage complex becoming ferritin
  • Ferritin releases stored Fe2+ converting itself back to apoferrin, iron goes into circulation as needed
82
Q

3 differentiated types of WBC progenitors from the hemocytoblast

A
  • B progenitors
  • T progenitors
  • granulocytes/macrophage colony forming units
83
Q

When thrombopoietin binds to a hemocytoblast, what happens?

A

It becomes a megakaryoblast by replicating DNA without nuclear or cytoplasmic cytokinesis

84
Q

How long to platelets survive in the circulation

A

5-9 days

85
Q

Erythropoietic growth factors/erythropoiesis stimulating agents function

A

Allow the patient to see increase in RBC count in patients with CRF and cancer patients undergoing chemotherapy

86
Q

Erythropoietic growth factors/erythropoiesis stimulating agents ADR’s (5)

A
  • Hypertension is most significant
  • Increased risk of DVT when used before elective surgery
  • Can worsen some cancers
  • cardiac arrest
  • autoimmune pure red cell aplasia (PRCA)
87
Q

Epoetin alfa (Epogen, procrit) class, therapeutic use,

A
  • Erythropoietic growth factor
    • can reverse anemia associated with CKD virtually eliminating need for transfusion
88
Q

Procrit indications (2)

A
  • treats chemo induced anemia in patients with nonmyeloid malignancies reducing need for transfusions
  • undergoing elective surgery when significant blood loss is expected
89
Q

Autoimmune pure red cell aplasia (PRCA) and treatment

A

Rare condition where treatment with epoeitin leads to a condition characterized by severe anemia and complete loss of erythrocyte precursor cells in bone marrow due to production of Abs directed against epoetin and native endogenous erythropoietin, which causes RBC production to cease, treatment consists of transfusions for survival

90
Q

Epoetin alfa administration and 2 drugs of this class

A

Injection
-epogen and procrit

91
Q

Darbepoeitin alfa (ARANESP) function

A

Long acting erythropoietin approved by FDA for treatment of anemia that has a slower clearance making half life 2-3x longer

92
Q

Darbepoeitin alfa (ARANESP) ADR’s (3)

A
  • Hypertension
  • MI
  • thrombosis
93
Q

Filgrastim (neupogen) OR Filgrastim-sndz (Zarxio) mechanism of action

A

Acts on cells of bone marrow to increase production of neutrophils using identical mechanism to G-CSF, and enhances phagocytic and cytotoxic actions of mature neutrophils

94
Q

Filgrastim (neupogen) OR Filgrastim-sndz (Zarxio) therapeutic uses (3)

A
  • Approved to reduce risk of infections in patients undergoing myelosuppressive chemotherapy (many chemotherapuetics suppress bone marrow, this leads to increased infection)
  • also used in bone marrow transplants and harvesting bone marrow
  • treats severe chronic neutropenia
95
Q

Filgrastim (neupogen) OR Filgrastim-sndz (Zarxio) administration

A

Injection IV or SC

96
Q

Pegfilgastrim (neulasta) characteristics

A

Long acting derivative of filgrastim (neupogen) that stimulates myeloid cells to increase neutrophil production, longer half life allows for treatment with one dose

97
Q

Pegfilgastrim (neulasta) ADR

A
  • devoid of serious ADR’s
    • bone pain
98
Q

Sargramostim (leukine, prokine) mechanism of action

A

Acts on cells in bone marrow to increase production of neutrophils, monocytes, macrophages and eosinophils by imitating a GM-CSF nearly identically

99
Q

Oprelvekin (Neumega) mechanism of action

A

Nearly identical to interleukin 11, increasing platelet production

100
Q

Romiplostim (Nplate) mechanism of action

A

Stimulates platelet production through acting as a thrombopoietin receptor agonist

101
Q

Kostmann’s syndrome

A

A severe congenital neutropenia

102
Q

Ferritin

A

Storage form of iron in mucosal and liver cells, apoferrin becomes this upon binding iron

103
Q

Trasnferrin

A

Iron binding protein for distribution throughout body

104
Q

Physiologic needs of iron require diet to contain ___ more iron than body needs because of how little is abosrbed (think about what the RDA represents)

A

10x

105
Q

Ferrous sulfate info and what is it DOC for?

A
  • Least expensive PO oral iron replacement therapy
    • DOC for iron deficiency anemias or sometimes used prophylactically
106
Q

Ferrous sulfate ADR’s (9)

A
  • nausea
  • heartburn
  • bloating
  • constipation
  • diarrhea
  • peptic ulcers
  • dark green stool
  • staining of teeth
  • toxicity
107
Q

Ferrous sulfate drug interactions (2)

A
  • Antacids reduce absorption
    • tetracyclines forms chelates decreasing absorption of both agents
108
Q

PO iron administration recommendation

A

Recommended to administer between meals, every other day per latest guidelines

109
Q

Ferrous gluconate/fumarate/aspartate function

A

Salts which are alternatives to ferrous sulfate, only difference is percent of iron content, produce same pharm effects, therapeutic responses, and ADRs

110
Q

Carbonyl iron function

A

Pure elemental iron in microparticles to enhance bioavailability and can be administered at an increased dosage safely (good for children)

111
Q

Iron dextran administration, function, indications

A
  • IV or IM, preferabely IV, Iron preparation consisting of ferric hydroxide and dextrans
  • reserved for those who cannot tolerate oral iron (such a those with intestinal disease or blood loss)
112
Q

B12 essential metabolic functions (2)

A
  • DNA synthesis
    • catalyze folic acid allowing for cell growth and division
113
Q

B12 absorption pathway

A
  • Requires intrinsic factor secreted by parietal cells of stomach to form complex
  • complex dissociates after absorption
  • transported by transcobalamin II into tissues
  • most B12 stored in liver, years to develop deficiency
114
Q

2 major causes of B12 deficiency

A
  • impaired absorption due to enteritis or celiac disease
    • lack of intrinsic factor (perhaps from gastric bypass!)
115
Q

Pernicious anemia

A

Atype of megaloblastic anemia where B12 deficiency due to lack of intrinsic factor resulting in low RBC count

116
Q

Erythroblasts are different from proerythroblasts in that they have ____

A

hemoglobin

117
Q

Anemia definition

A

Decrease in erythrocyte number, size, or hemoglobin content either due to blood loss, hemolysis, bone marrow dysfunction, or nutritional deficiences

118
Q

During pregnancy, what happens to iron requirements?

A

They increase very high, often requiring supplementation

119
Q

Vegans run the risk of this vitamin deficiency because it is only obtained from animal products or fortified foods

A

B12

120
Q

Cyanocobalamin B12 function and DOC for what?

A

Purified crystalline form of vit B12 and DOC for B12 deficiency

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