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NUNP531 Applied Pathophysiology > FINAL endocrine > Flashcards

FINAL endocrine Flashcards

1
Q

Metabolic syndrome - what does this group of disorders encompass? What are the risks of this syndrome?

A

Highly prevalent, multifaceted condition characterized by a constellation of abnormalities that include abdominal obesity, hypertension, dyslipidemia and elevated BG.

Together give a high risk of development type 2 diabetes and associated cardiovascular complications.

*Metabolic syndrome and type 2 diabetes can also coexist

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2
Q

Metabolic syndrome is considered a pro_________and pro________ state.

A

proinflammatory and prothrombotic state.

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3
Q

Metabolic syndrome requires 3 or more of 5 criteria. What are the criteria?

A

1) Elevated waist circumference (cm) for Canada: > (or equal to)102cm for men, 88cm for women
2) Elevated triglyceride (TG) mmol/L > or equal to 1.7mmol/L (for men and women)
3) Reduced HDL-C <1.0, <1.3 (for men and women)
4) Elevated BP (mmHg) systolic > (or equal to) 130 or diastolic > (or equal to) 85
5) Elevated fasting glucose (mmol/L) > (or equal to) 5.6

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4
Q

Epidemiology of metabolic syndrome - what population is this growing in?

A

*Increased age

*Canada-incidence is estimated at 19.1% of the population

*Increasing in children & adolescents’ d/t to increased rates of obesity

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5
Q

Patho of metabolic syndrome. How does this lead to CV disease?

A

*The exact etiology is unknown

*Vascular endothelial dysfunction occurs secondary to insulin resistance, hyperglycemia, hyperinsulinemia, and adipokines.

*Along with high blood pressure (BP) and abnormal lipids, vascular inflammation places the individual at high risk of a CV insult.

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6
Q

Complications associated with metabolic syndrome include:

A

-Fatty liver disease
-Cirrhosis
-Chronic kidney disease
-CV disease
-Polycystic ovarian syndrome (PCOS)
-Obstructive sleep apnea (OSA)
-Gout

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7
Q

Which two presentations are considered the strongest predictors for the development of metabolic syndrome.

A

Elevated triglycerides and waist circumference.

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8
Q

What is the treatment plan for a patient who has been diagnosed with metabolic syndrome?

A

*Identify and treat pt with hyperglycemia

*Management of hypertension, dyslipidemia and abdominal obesity

*Diet modification, exercise (minimum 30min/day), weight loss, smoking cessation

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9
Q

List all the hormones released by the anterior pituitary

A

FSH, LH, TSH, MSH, GH, Prolactin

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10
Q

____ forms the structural and functional basis of the neuroendocrine system

A

the hypothalamic-pituitary axis!

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11
Q

What effects does the HPA have?

A

directly affects functions of thyroid gland, adrenal gland and gonads, as well as influencing growth, milk production and water balance

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12
Q

What part of the brain is considered the coordinating system of the endocrine system?

A

The hypothalamus

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13
Q

Where is hypothalamus located? What structure connects it to the pituitary?

A

Located at base of the brain, connected to pituitary gland by pituitary stalk

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14
Q

How does the hypothalamus talk to the anterior pituitary vs the posterior pit?

A

Connected to anterior pituitary by hypophysial portal blood vessels –> communicates via BLOOD SUPPLY to induce release of hormones

Connects to posterior pituitary via a nerve tract –> communicates via NERVE SIGNALS to induce release of hormones

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15
Q

T/F The posterior pituitary makes its own hormones.

A

Posterior does NOT make its own hormones (just stores & releases ADH & oxytocin)

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16
Q

What is the deal with neurosecretory cells in the hypothalamus?

A

Has neurosecretory cells that are similar to other neurons but can synthesize & secrete the hypothalamic-releasing hormones that regulate release of hormones from the anterior pituitary

These neurosecretory cells also synthesize ADH & oxytocin

Hypothalamic hormones have special circulation so that they reach their target cells in the pituitary in high concentrations

These hormones are small peptides that are generally active only at the relatively high concentrations achieved in the pituitary portal blood system

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17
Q

Overall fx of the hypothalamus in hormone regulation…

A

Consolidates signals from upper cortical inputs, autonomic function, environmental cues such as light and temperature and peripheral endocrine feedback

Delivers precise signals to the pituitary gland

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18
Q

What is considered the “master gland”

A

Pituitary

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19
Q

What are the risk factors for DMT2?

(answers taken from the Diabetes Canada CPGs)

A

Assess risk factors for type 2 diabetes ANNUALLY:
* Family history (first-degree relative with type 2 diabetes)
* High risk populations (non-white, low socioeconomic status)
* History of GDM/prediabetes
* Cardiovascular risk factors
* Presence of end organ damage associated with diabetes

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20
Q

Which lab results are used when screening for DMT2?

A

FBG (at least 8 hours post-prandial):
6.1 – 6.9 Impaired fasting glucose -> prediabetes
≥7.0 Diabetes

A1C (%):
6.0 – 6.4 Prediabetes
≥6.5 Diabetes

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21
Q

What is the recommended A1C target for adults with DMT2?

A

A1C% Targets
≤6.5 Adults with type 2 diabetes to reduce the risk of CKD and retinopathy if at low risk of hypoglycemia*
≤7.0 MOST ADULTS WITH TYPE 1 OR TYPE 2 DIABETES

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22
Q

For which populations are higher target A1C percentages acceptable? (7.1-8.5%)

A

Functionally dependent: 7.1-8.0%

Recurrent severe hypoglycemia and/or hypoglycemia unawareness: 7.1-8.5%

Limited life expectancy: 7.1-8.5%

Frail elderly and/or with dementia: 7.1-8.5%

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23
Q

What are the recommended things to review regularly with your patients diagnosed with DMT2?

A

Regular Review:
* Assess glycemic control, cardiovascular and renal status
* Continue to screen for complications
(eyes, feet, kidney, heart)
* Review efficacy, side effects, safety and ability to take
current medications
* Reinforce and support healthy behaviour interventions

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24
Q

What are the ABCDESSS of DMT2 management?

A

A - A1C targets (≤7.0%)
B - BP targets (<130/80)
C - Cholesterol targets (LDL <2.0)
D - Drugs for CV and/or
Cardiorenal protection
E - Exercise goals and
healthy eating
S - Screening for complications
S - Smoking cessation
S - Self-management, stress, other barriers

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25
Q

What causes DMT2?

A

The pancreas does not produce enough insulin, or the body does not effectively use the insulin that is produced.

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26
Q

What does PCOS stand for?

A

Polycystic ovary syndrome - one of the most common endocrine disturbances affecting women

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27
Q

Which hormones are altered in PCOS?

A

Androgens – an excess

LH - high

FSH - low

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28
Q

Patients must meet at least 2 of 3 criteria for diagnosing PCOS. What are the three criteria?

A

Few or anovulatory menstrual cycles

Elevated levels of androgens

Polycystic ovaries

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29
Q

Do polycystic ovaries need to be present in order to diagnose PCOS? Do polycystic ovaries alone establish a diagnosis of PCOS?

A

no and no

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30
Q

Be careful not to confuse PCOS with _______

A

Benign ovarian cysts. Different pathophysiology

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31
Q

Outline the patho of PCOS

A

Direct cause related to a genetic predisposition and an obesity-prone lifestyle related to insulin resistance and an excess of glucose and androgens

Hyperandrogenic state is a cardinal feature. Glucose intolerance and hyperinsulinemia often occur concurrently and markedly aggravate the hyperandrogenic state, thus contributing to the severity of PCOS

Insulin resistance and resultant compensatory hyperinsulinemia overstimulates androgen secretion by the ovarian stroma

Excessive androgens affect follicular growth and insulin affects follicular decline by supressing apoptosis and enabling the survival of follicles that would normally disintegrate

Seems to be a genetic ovarian defect that makes the ovary more susceptible to insulin stimulation of androgen production

FSH is usually low and LH elevated. LH elevation causes increased concentration of androgens, which are converted to estrogen in peripheral tissues. Elevated estrogen levels cause a positive feedback loop in LH and negative in FSH.

Because FSH is not totally depressed, new follicular growth is continuously stimulated, but not to full maturation and ovulation

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32
Q

When does PCOS usually begin?

A

Clinical manifestations usually appear within two years of puberty, but may appear after a period of normal menstrual function and pregnancy

33
Q

S/S of PCOS

A

S/S are related to anovulation and hyperandrogenism

DUB (dysfunctional uterine bleeding) or amenorrhea, hirsutism, acne, infertility, obesity

34
Q

What are other disorders associated with PCOS

A

Hypertension, dyslipidemia, diabetes (including gestational), other endocrine disorders, endometrial hyperplasia and carcinoma, preterm birth, perinatal mortality

35
Q

Diagnosis of PCOS is based partially on evidence of androgen excess – what are some examples?

A

Hirsutism, male pattern hair distribution, acne

Also look for irregular menstrual patterns, insulin resistance and low FSH/high LH

36
Q

Treatment for PCOS

A

Combined oral contraceptives – controls irregular menstrual cycles and opposes estrogens and androgens

Metformin – may be used to decrease insulin resistance, prevent diabetes and heart disease and restore fertility

Reduction in weight can dramatically improve insulin sensitivity and return of ovulatory cycles

37
Q

What is TSH?

A

Regulates the activity of the thyroid gland
Circulates to bind with receptors of thyroid follicular cells
Causes release of stored thyroid hormone (T3, T4) and increased TH creation
Increases growth of thyroid gland by stimulating thymocyte hyperplasia and hypertrophy

38
Q

Where is TSH created, stored, and released from?

A

Anterior pituitary

39
Q

What increases TSH secretion?

A

Low levels of T3, T4 > TRH thyroid releasing hormone secreted > stimulates TSH secretion

40
Q

What inhibits TSH secretion?

A

High levels of T3/ T4 (negative feedback loop)

41
Q

Where is TRH created, stored, and released from?

A

Hypothalamus

42
Q

Describe the feedback loop of the thyroid. Is it positive or negative?

A

Negative feedback loop- involves the hypothalamus, anterior pituitary, and thyroid.
Low levels of TH sensed by hypothalamus, which releases TRH to stimulate the anterior pituitary to release TSH. This stimulates follicular cells to release TH (T3 and T4). Once released into circulation, TH are transported by thyroxine binding albumin, pre albumin, or lipoproteins. Only the unbound form is active.

43
Q

Is T4 or T3 more readily produced? What’s the difference?

A

T4. Has 4 iodine molecules bound instead of 3. In the tissues, T4 converts to T3, which acts on the target cell.

44
Q

What makes TH?

A

Follicular cells in the thyroid

45
Q

What is primary vs. secondary hypothyoidism?

A

Primary: deficient production of TH by thyroid gland. Low TH, high TSH.
Secondary: Pituitary does not synthesize TSH, or lack of TRH. Low TH, Low TSH.

46
Q

What is the most common cause of primary hypothyroidism?

A

Hashimoto’s (autoimmune thyroiditis)

47
Q

Diagnostic criteria for hypothyroidism?

A

Low TH, high TSH

48
Q

Diagnostic criteria for sub clinical hypothyroidism?

A

Normal TH, high TSh

49
Q

Diagnostic criteria for hyperthyroidism?

A

High TH, low TSH

50
Q

Diagnostic criteria for sub clinical hyperthyroidism?

A

Normal TH, low TSH

51
Q

Interpret the following lab results. No s/s.
TSH 2.2 (0.32- 5.04), T4 13.5 (10.6- 19.7).

A

Normal TSH, normal T4- euthyroid :)

52
Q

Interpret the following lab results. No s/s.
TSH 12 (0.32- 5.04) and T4 8 (10/6-19.7)

A

High TSH (Don said the “cut off” for when we confidently call it elevated is 10)
Low T4

Hypothyroidism (primary).

53
Q

Interpret the following lab results. No s/s
TSH 6 (0.32- 5.04), T4 15 (10.6- 19.7)

A

Slightly high TSH (still less than 10)
Normal T4

Subclinical hypothyroidism

54
Q

Interpret the following lab results. Pt has palpitations.
TSH 0.2 (0.32- 5.04), t4 33 (10.6- 19.7)

A

TSH low
TH high

Hyperthyroidism

55
Q

What are some considerations re: levothyroxine?

A

Take consistently (it binds to many things). Empty stomach preferred.
Caution in older patients/ those with heart disease- TH increases metabolism, increasing myocardial o2 demand- can result in ischemia/ injury

56
Q

Patient with hypothyroidism presents for lab results. On levothyroxine.
Has lost 15 pounds in 3 months through diet and exercise
Lab results: TSH 0.3 (0.32- 5.04) and T4 18 (10.6- 19.7)
What is your interpretation of thyroid function, and what would you do with her levothyroxine dose?

A

TSH low.
T4 normal.
Subclinical hyperthyroidism.
Decrease levothyroxine dose.

57
Q

Patient with hypothyroidism presents for lab results. On levothyroxine. Has gained 15 pounds. TSH 6 ( 0.32- 5), T4 16 (10-19)
Interpretation of thyroid function, what would you do with her levothyroxine dose?

A

TSH slightly high
TH normal
Increase levothyroxine dose

58
Q

Risk factors for hypothyoidism

A
  • Family history of thyroid dysfunction
  • Diagnosis of autoimmune disease
  • Age >50F >60M
  • Gender: female
  • Postpartum
  • Hyperthyroid treatment
  • Radiation to the head or neck
  • Drug therapies such as lithium and amiodarone
  • Dietary factors (iodine is required for the synthesis of TH)
  • Chromosomal or genetic disorders (e.g., Turner syndrome, Down syndrome, and mitochondrial disease) (BC guidelines, 2018).
59
Q

The most common cause of hypothyroidism is ____________

A

hashimoto’s thyroiditis

60
Q

Describe the patho of hashimotos

A

Autoimmune disorder where autoreactive t cells and circulating antibodies target and infiltrate the thyroid, resulting in gradual inflammatory destruction. Loss of thyroid function leads to lack of negative feedback on hypothalamus/ pituitary. Results in elevated TRH, TSH, and decreased TH.

Low TH- slowing of metabolic processes, myxedema.

Overstimulation of thyroid by excess TSH can lead to goitre

61
Q

Other causes of hypothyroidism?

A

hyperthyroid treatment, head and neck radiation, medications, congenital defects, and iodine deficiency

62
Q

Signs and symptoms hypothyroidism?

A

Metabolism: Low metabolic rate, weight gain, cold intolerance, and slightly lowered basal body temperature.
Neuro: Lethargy, fatigue, memory or mental impairment, difficulty concentrating, and slowed speech or thinking.
Thyroid: normal, small, or increased (Goitre).
Cardio: Bradycardia, hypertension, pericardial effusion.
Resp: SOB, Pleural effusion.
GI/Repro: Constipation, heavy or irregular menstrual periods.
Skin: Dry and flaky skin. Course and brittle hair with possible loss. Myxedema: Characteristic sign of severe or longstanding hypothyroidism. Usually seen in the eyes, hands, feet, and supraclavicular fossa. The tongue and laryngeal and pharyngeal mucous membranes can also thicken, producing thick, slurred speech and hoarseness.
MSK: Delayed deep tendon reflexes, muscle aches, and paresthesia to hands and feet.
Myxedema coma: Severe hypothyroidism. Mortality 30-50%. Usually occurs in undiagnosed or untreated hypothyroid patients, and can be precipitated by an acute event.

63
Q

Diagnosis hypothyroidism?

A

Labs: high tsh, low t4, anti-TPO (antithyroid anti body- can help determine if hashimotos is the case).

US can be used to eval abnormal gland.

CT or MRI in the case of secondary causes.

64
Q

Tx hypothyroidism?

A

thyroxine (t4)- weight based dosing, labs q6weeks until correct dosage determined, then at least annually. overdose= s&S hyperthyroidism. hormone levels can fluctuate amd dosage may need to be titrated. Many foods alter absorption.

endocrinology if pregnant, goitre, nodules, pituitary dusfunction, cardiac disease

65
Q

T/F subclinical hypothyroidism has no symptoms.

A

True or may have vague non specific symptoms (i.e.. fatigue and constipation)

66
Q

Consequences of subclinical hypothyroidism?

A

Increased CVD risk, and progression to hypothyroidism

67
Q

Dx subclinical hypothyroidism

A

labs- high TSH, normal T4

68
Q

Treatment subclinical hypothyroidism

A

TREAT IF TSH > 10 + symptoms, evidence of atherosclerotic hear disease, CHF, risk factors for these diseases, or pregnancy. Monitor if not treating.

69
Q

Risk factors hyperthyroidism?

A

-Risk factors for thyroid disease: men age >60 years, women age >50 years, personal history of strong family history of family thyroid disease, diagnosis of other autoimmune disease, hx neck radiation, previous thyroidectomy or radioactive iodine ablation, drug therapies like lithium or amiodarone (thyrotoxicosis) dietary factors (i.e., iodine excess), chromosomal disorders (turners, downs, mitochondrial disease), pregnancy (post partum thyroiditis- dt modulation of immune system)

70
Q

What is more common: hypo or hyper thyroid

A

hypo

71
Q

Patho of hyperthyroidism

A

Excess secretion of TH from thyroid gland

72
Q

Most common cause of hyperthyroid?

A

Graves

73
Q

Describe patho of graves disease

A

Autoimmune, type II hypersensitivity
Stimulation of thyroid of autoantibodies directed against TSH receptor.
Results in hyperplasia of gland (goitre) and increased creation of TH (esp T3). Increased TH results in s&S hyperthyroidism. Inhibition of TSH through normal feedback loop.

74
Q

What can also cause hyperthyroidism?

A

Nodular thyroid disease: Thyroid gland enlarged in response to increased demand for SH (i.e., puberty, pregnancy, iodine deficiency). When the condition resolves, TSH secretion normally subsides and the thyroid gland returns to its original size
* Irreversible changes can occur in some follicular cells, which will cause them to function autonomously and produce excessive TH
-toxic multinodular goitre (several hyperfunctioning nodules) (no autoimmune stimulus)
-toxic adenoma (only 1 nodule hyperfunctioning)
* Usually develops slowly
* Incidence of malignancy is 9%

75
Q

S&S hyperthyrodism?

A
  • Neuropsychiatric (anxiety, irritable, restless, fatigue, increased appetite, decreased attn span
  • Neuromuscular (tremors, proximal muscle weakness, hyperreflexia)
  • Physical appearance/ voice (weight loss, hair loss/ thinning)
  • Cardiovascular (tachycardia, palpitations, afib, systolic HTN, HF)
  • Thyroid gland (goitre)- enlargement of thyroid gland (goitre) common in conditions caused by stimulation of TSH receptors- diffuse, warm on palpation, nodular (or solitary toxic nodule)
  • Thermoregulation (increased sweating, sweaty palms, heat intolerance, warm skin)
  • Ophthalmologic (blurred or double vision, dry eyes, conjunctivitis, proptosis or deconjugate gaze)
    Exophthalmos (protruding eyes)
    -graves disease: can have functional abnormalities of eye resulting from hyperactive SNS (lag of globe on upward gaze and upper lid on downward gaze) and infiltrative changes involving orbital contents with enlargement of ocular muscle> connective tissue, inflammation, edema> results in visual problems, exophthalmos, periorbital edema, diplopia, pain, lacrimation, photophobia, corneal ulceration.
    -***not present in nodular thyroid disease
  • GI (diarrhea)
  • Pituitary (amenorrhea or oligomenorrhea)
  • Skin (pretibial edema_
    -graves disease: very high levels of autoimmune antibodies- cutaneous swelling on anterior legs and indurated, erythematous skin
    -***not present in nodular thyroid disease
76
Q

Diagnosis hyperthyroidism?

A

Elevated TH and low TSH

77
Q

Tx hyperthyroidism

A

production, secretion, or action
-antithyroid medication
-radioactive iodine therapy (absorbed only by thyroid tissue, causing death of cells)
-surgery
*complication > hypothyroidism
-nodular thyroid disease requires biopsy of suspicious nodules before treatment; treatment= radioactive iodine, surgery, antithyroid meds

Monitoring:
-allow 1+ month before repeated TSH and TH levels (as pituitary secretion of TSH may be low/ supressed for long periods following hyperthyroidism)
-until TSH resolves, base treatment/ dosing decision on T4

78
Q

Summarize thyroid feedback loop

A

Hypothalamus releases TRH which acts on anterior pituitary to cause release of TSH, which acts on thyroid (follicular cells) to increased production of TH (T4 and T3), which is released into circulation (travelling on lipoproteins or albumin) and acts as T3 in tissues. High TH provides negative feedback preventing further release of TRH, stopping excess TH production.
Low TH provides negative feedback causing release of TRH so more TH is eventually made.

NUNP531 Applied Pathophysiology (24 decks)

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