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Patho > Week 10 Endocrine > Flashcards

Week 10 Endocrine Flashcards

1
Q

Explain the hormone classifications and the hormones that are in each one

A

Amines (derived from amino acids)
- epinephrine, dopamine, T2 and T4

Peptide hormones (proteins, glycoproteins) 
- insulin, glucagon, hypothalamus and pituitary hormones

Steroid hormones (made from cholesterol)

  • cortisol, aldosterone, testosterone
  • all of the steroid hormones come from adrenals

Eicosanoids (made from fatty acids)
- prostaglandins, leukotrienes, thromboxane’s

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2
Q

What do the endocrine glands affect

A

distant target cells

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3
Q

What do paracrine cells affect

A

nearby target cells

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4
Q

what do autocrine cells affect

A

they secrete compounds that stimulate themselves

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5
Q

Explain up-regulation and down-regulation

A

up-regulation: decreased hormone levels often produce an increase in receptor numbers by means of a process; increases sensitivity

down-regulation: sustained levels of excess hormone often bring about a decrease in receptor numbers; decrease in hormone sensitivity

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6
Q

Explain the hormones that come out of the posterior and anterior pituitary

A

Posterior:

  • ADH
  • Oxytocin
  • interior hypophyseal artery

Anterior:

  • growth hormone
  • TSH
  • ACTH (which will then lead to release of cortisol)
  • FSH
  • LH
  • Prolactin
  • MSH (she didn’t know what this was so not very important)
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7
Q

Explain the hypothalamus pituitary axis

A
  • blood flow drains into the anterior pituitary gland

- nerve axons feed the posterior pituitary gland

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8
Q

What things does the hypothalamus detect

A
  • temperature
  • blood osmolarity
  • blood nutrients
  • blood hormone levels
  • inflammatory mediators in blood
  • emotions
  • pain
  • releases xxx-releasing hormone
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9
Q

What feedback loop does the hypothalamus use to maintain all concerns

A

negative feedback loop

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10
Q

Explain positive and negative feedback loops

A

Negative feedback system:

  • functions like a thermostat
  • on going, fine tuning and maintenance

Positive feedback:

  • uterine contractions
  • these have to terminate on their own somehow so they are self-limiting (ex. when the baby is delivered)
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11
Q

What are the diagnostic tests you can run with GI/GU issues

A

Blood tests:
- hormones, antibodies, regulated substance (blood glucose)

Urine tests:
- hormones or hormone metabolites

Stimulation tests:
- to diagnose hypofunction (no response from endocrine gland is worrisome)

Suppression tests:
- to diagnose hyperfunction (looking to see if the endocrine gland is overactive)

Genetic tests

Imaging studies:
- isotopic imaging, MRI, CT, ultrasound, PET, DEXA

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12
Q

Explain what the anterior pituitary hormones stimulate

A
  • ACTH stimulates the adrenal cortex which leads to cortisol
  • TSH stimulates the thyroid which leads to thyroid hormones
  • GH stimulates the liver which leads to IGF-I
  • FSH and LH stimulate gonads which leads to sex hormones
  • Prolactin stimulates the breast which leads to milk production
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13
Q

Explain the general aspects of altered function, specifically hypofunction and hyperfunction

A

Hypofunction:

  • impaired/damaged gland
  • inadequate or ineffective hormone (making them but they don’t work)
  • damaged, missing, or ineffective receptors

Hyperfunction:

  • paraneoplastic syndromes (tumor releases things that look like hormones but are not)
  • exogenous hormones (Ex: taking prednisone for a long time which is an example of an exogenous hormone)
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14
Q

Explain the different hormone disorders

A

Primary:

  • abnormally in the peripheral gland
  • target gland hormone
  • target gland is broken (ex. thyroid doesn’t respond to TSH)

Secondary:

  • abnormality in the anterior pituitary (pituitary is broken)
  • tropic hormone

Tertiary:

  • abnormality in the hypothalamus
  • releasing hormone
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15
Q

Explain pituitary disorders. What is the common cause? Explain hypopituitarism

A

Can be hypo- or hypersecretion

  • localized mass effect that causes compression of optic chiasm which leads to vision changes
  • pituitary is highly vascular so at increased risk for ischemic injury

Common cause:

  • neoplasms
  • pituitary adenoma is common in adults which leads to hyperpituitarism
  • prolactin secreting tumors are the most common

Hypopituitarism
- can involve one subset or all (panhypopituitarism)

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16
Q

Explain the consequences of GH deficiency and excess before and after puberty

A

GH Deficiency:

  • before puberty: dwarfism
  • after puberty: somatopause, associated with metabolic disease, tumors

GH Excess:

  • before puberty: gigantism (growth plate hasn’t fused)
  • after puberty: acromegaly (thickening of bone; specifically in face)
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17
Q

What are thyroid hormones required for

A

metabolism (#1 of importance), cardiorespiratory function, GI function, neuromuscular function

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18
Q

Explain T3 and T4 hormones. What are they released by?

A
  • released by the thyroid
  • both are carried by binding proteins (individuals that are malnourished can have issues with this)
  • iodine is required for adequate thyroid function
  • T3 stimulates metabolism (T4 is inactive until converted into T3 in tissues)
  • both exert negative feedback
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19
Q

Explain hypothyroidism. Explain the 2 main factors for the manifestations

A
  1. Congenital vs. acquired
    - hashimoto thyroiditis (10% of pregnancies result in subacute)
    - Thyroidectomy (hypoPTH)

Manifestations due to 2 main factors:

  • hypometabolic state
  • Myxedema is an accumulation of a hydrophilic mucopolysaccharide substance (tissue collects fluids which causes a unique type of edema)
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20
Q

What are the common causes of hyperthyroidism?

A
  • Graves’ disease and diffuse goiter

- antibodies land on receptor and overstimulate it

21
Q

Explain Graves’ Disease

A
  • type 2 hypersensitivity
  • autoimmune
  • Triad: hyperthyroidism, goiter, exophthalmos
  • pretibial myedema
22
Q

Explain the thyroid storm (or crisis) that could occur with hyperthyroidism

A
  • an acutely exaggerated manifestation of the thyrotoxic state
  • tachycardia and palpitations
23
Q

Explain primary and secondary hyperparathyroidism

What are the clinical manifestations

A

Primary:

  • primarily due to parathyroid adenoma (80-85%) or parathyroid hyperplasia (10-15%)
  • hypercalcemia, hypercalciuria, hyper phosphaturia, alkaline urine which leads to calcium oxalate kidney stones

Secondary:

  • chronic renal disease or malabsorption cause a decrease in serum calcium
  • hypercalcemia does not occur (labs will be on the low end of normal)

Clinical manifestations:
- excessive osteoclastic lead to pathologic bone fractures

24
Q

Explain hypoparathyroidism

what electrolyte disturbances will occur

A
  • most commonly caused by damage to parathyroid glands during thyroid surgery
  • hypomagnesemia (related to alcohol, malnutrition, malabsorption, parenteral nutritional therapy)

Electrolyte disturbances:

  • calcium will be low
  • hypocalcemia manifestations: twitchy people
25
Q

What are the three types of hormones produced by the adrenal cortex

A
  • mineralocorticoids (aldosterone)
  • glucocorticoids (mainly cortisol)
  • adrenal androgens (DHEA - metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids)

Anytime you mess with one of these, you sort of mess with all since they all come from adrenal cortex

26
Q

Explain the adrenal cortical hormone disorders that occur when cortisol increases and suppresses

A

Cortisol increases:

  • plasma proteins
  • catabolism
  • muscle breakdown
  • free fatty acids
  • blood glucose
  • SNS response

Cortisol suppresses:
- the immune and inflammatory systems.

27
Q

What are the two types of adrenal cortical disorders

A
  • congenital adrenal hyperplasia

- adrenal cortical insufficiency

28
Q

Explain the three types adrenal cortical insufficiency

A
  1. Primary adrenal insufficiency (Addison disease)
    - TB is a major cause
    - mineralocorticoid deficiency (aldosterone), glucocorticoid, and hyperpigmentation (due to increase ACTH)
  2. Secondary adrenal insufficiency
    - hyperpigmentation not present (pituitary is broken)
    - common cause due to rapid withdrawal of steroids
  3. Acute adrenal crisis
29
Q

What does Cushing syndrome refer to? What are the three forms

A

Cushing syndrome refers to the manifestations of hypercortisolism from any cause to include exogenous steroids

  • Pituitary form: cushing disease = excessive production of ACTH by a tumor of the pituitary gland
  • Adrenal form: benign or malignant adrenal tumor
  • Ectopic form: results from a paraneoplastic syndrome; coming from the wrong source; tumor releasing the hormones
30
Q

What are the types of diabetes mellitus

A
  • Type 1A: autoimmune destruction of pancreatic beta cells
  • Type 1B: idiopathic diabetes
  • Type 2: beta cell dysfunction and insulin resistance
  • Gestational diabetes mellitus
  • other specific types of diabetes: genetic effects in beta cell function, diabetes secondary to other diseases, drugs, or transplant
31
Q

Explain type 1 diabetes. How many beta cells must be loss before an individual becomes symptomatic?

A
  • autoimmune mediated loss of beta cells in the pancreatic islets
  • slowly progressive autoimmune T-cell-mediated disease that occurs in genetically susceptible individuals (they destroy their own beta cells)
  • 80 - 90% loss of beta cells must occur before symptomatic
  • Sx include hyperglycemia, glucagon, and hyperketonemia
  • in absence of insulin, ketosis develops when free fatty acids and converted to ketones in the liver
  • cannot give these individuals oral hypoglycemics
32
Q

Explain multifactorial disease with type 2 diabetes

A
  • genetic predisposition but also environmental

- altered adipokines expression in obese individuals

33
Q

What type of diabetics does metabolic syndrome typically occur in? What are the other factors that can cause metabolic syndrome?

A
  • hyperglycemia typically in DM2

Other factors include:

  • intra-abdominal obesity
  • increased blood triglyceride levels (>150 mg/dL)
  • increased blood pressure (>130/85)
  • systemic inflammation
34
Q

What are the acute complications of diabetes mellitus

A
  • diabetic ketoacidosis
  • hyperglycemic hyperosmolar state
  • hypoglycemia
  • somogyi effect
  • dawn phenomenon
35
Q

What are the 3 Ps of diabetic ketoacidosis

A

polydipsia, polyuria, polyphagia

36
Q

Why do individuals with diabetic ketoacidosis experience polyphagia

A

they are hungry because they are not breaking down the glucose they have so the body thinks it needs more

37
Q

Why do individuals with diabetic ketoacidosis experience polyuria

A

The kidneys are pulling H2O due to increase in osmotic pull. the kidneys are trying to pull water from the vascular space because the large sugar molecules are spilling over

38
Q

Explain why individuals with diabetic ketoacidosis will experience polydipsia

A

they are thirsty due to cells becoming dehydrated intracellularly and intravascularly

39
Q

What type of diabetics are more likely to develop diabetic ketoacidosis

A
  • type 1 diabetics are more likely to develop because they don’t have insulin
40
Q

What is the main difference between DKA and HHNKS

A

in HHNKS (typical with type 2 diabetes) they still have some insulin but still have way too much sugar

41
Q

What is considered low blood sugar? What do symptom presentations related to?

A

<45 to 60 mg/dl

symptom presentation is related to rate of decline (faster rate = more symptomatic)

42
Q

What are the adrenergic and neuroglycopenic symptoms of hypoglycemia

A

Adrenergic symptoms:

  • tachycardia
  • palpitations
  • diaphoresis
  • tremors
  • pallor
  • anxiety

Neuroglycopenic symptoms:

  • headaches
  • dizziness
  • irritability
  • fatigue
  • poor judgement
  • confusion
  • visual changes
  • seizures
  • coma
43
Q

Explain the somogyi effect

A
  • hypoglycemia with rebound hyperglycemia
  • they have a drop in sugar then the body tries to fix it but they overshoot the mark
  • most common in persons with type 1 diabetes mellitus and in children
44
Q

Explain the dawn phenomenon

A
  • early morning glucose elevation without nocturnal hypoglycemia
  • related to nocturnal growth hormone elevation
  • hypoglycemic and body tries to fix it but body overshoots the mark so they wake up every morning with elevated sugar
45
Q

Explain the 2 buckets that chronic complications of diabetes mellitus

A

Microvascular issues:

  • due to the thickening of the capillary basement membrane, endothelial cell hyperplasia, and thrombosis which leads
  • leads to diabetic neuropathies, nephropathies, and retinopathies

Macorvascular issues:

  • Cerebrovascular accident (stroke), coronary artery disease, peripheral vascular disease, atherosclerosis
  • diabetic foot ulcers (#1 cause of nontraumatic amputations)
  • infections
  • bigger vessels affected
46
Q

Explain the two types of diabetic neuropathies

A

Somatic neuropathy:

  • diminished perception: vibration, pain and temperature
  • hypersensitivity: light touch; occasionally severe ‘burning’ pain (paresthesia pain)

Autonomic neuropathy:

  • defect in vasomotor and cardiac responses (someone could be having a heart attack and not know it)
  • inability to empty the bladder (due to neuropathies)
  • impaired motility of the GI tract
  • sexual dysfunction (due to blood flow, PVD, CAD)
47
Q

What are the reasons that the risk of infection increases with diabetic

A
  • impaired senses
  • hypoxia due to micro and macrovascular issues
  • rapid replication of pathogens from increased glucose
  • decreased blood supply
  • suppressed immune response
  • delayed wound healing
  • poor healers
48
Q

What are the adaptations the body does in response to stress

A
  • time (fast vs slow)
  • genetic endowment
  • age and gender
  • health status
  • nutrition
  • sleep wake cycles
  • hardiness
  • psychosocial
49
Q

What are the results of long term stress, specifically chronic stress, PTSD, and major depression

A

Chronic stress:

  • sympathetic activity and cortisol elevated
  • complications results from reduced immune response

Posttraumatic stress disorder:

  • the sympathetic system is activated
  • cortisol levels are decreased (body begins to respond differently due to the chronic changes)

Major depression:
- HPA theory (didn’t really address this in lecture)

Patho (10 decks)

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