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Patho Test 4 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are some possible pathologies in the endocrine system?

A
  • Hyperfunction – too much hormone
  • Hypofunction – too little hormone
  • Tumors/cancer
    • Often cause hyperfunction
    • Sometimes cause Bulk disturbance
      • pressure on adjacent cells by tumor → cells no longer produce hormones → lead to hypofxn
  • Defective Receptor or Enzyme
    • associated with genetic disease, autoimmune
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2
Q

What can cause elevated or depressed hormone levels?

A
  • Failure of feedback systems
    • Issue with negative feedback loops → hyperproduction
    • Issue with gland
  • Dysfunction of an endocrine gland – ie bulk tumor, CA
  • Secretory cells are unable to produce, obtain, or convert hormone precursors – ex: genetic dx
  • The endocrine gland synthesizes or releases excessive amounts of hormone
  • Increased hormone degradation or inactivation - Autoimmune
  • Ectopic hormone release
    • Ex: lung CAs releasing ACTH
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3
Q

What is target cell failure in relation to endocrine disorders?

A
  • Receptor-associated disorders
    • Decrease/increase in number of receptors
    • Impaired receptor function - Autoimmune (AI)
    • Presence of antibodies against specific receptors - AI
    • Antibodies that mimic hormone action
      • Ex: Graves Disease (hyperthyroidism)
        • Antibody mimics TSH & cause ­increase TH production
    • Unusual expression of receptor function – genetic malfunction
      *
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4
Q

Cause of hyperthyroidism?

A
  • Graves disease
    • ** most common** (autoimmune)
  • Hyperfunctioning adenoma (toxic goiter)- impacts airway
  • TSH cell adenoma
    • TSH over functioning → increase­ feed forward system (TSH stimulating thyroid gland to produce more TH)
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5
Q

Cuases of hypothyroidism?

A
  • Hashimoto thyroiditis
    • ** most common **in developed countries
    • caused by an autoimmune disorder
  • Iodine deficiency
    • **most common worldwide**
    • Other countries don’t iodize salt (US adds iodine to salt)
  • Ablation
    • Ex: parathyroid gland sx (sits right next to TG)
      • can have accidental ablation of TG itself
      • sx on PTG → send cells for frozen sections to ensure removal of only PTG
  • Idiopathic
    • no known causes, aging
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6
Q

What are some carcinomas that result in thyroid pathologies?

A
  • Carcinomas – can cause bulk disturbances or overproduction
    • Papillary
    • Follicular
    • Medullary
    • Anaplastic
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7
Q

What are the thyroid hormones? Testing for thyroid hormones?

A
  • T4:T3 ratio 10:1
    • Much more T4 produced → converted to T3 in periphery
  • T3 is 3-4X more active/potent than T4
  • Testing:
    • Third generation of TSH assay (TSH3)- (HIGHLY sensitive)
      • TSH3 can measure levels below 0.020 mIU/L (Normal 0.4-2.5)
      • Used to distinguish the extremely low levels of TSH suppression of Graves’ disease from the less severely suppressed TSH of non-thyroid illness
        • (this test is useful in helping diagnosis Graves’—main reason people become hypothyroid)
  • Small changes in function of TSH can lead to significant changes in TSH secretion
    • Anytime there’s even a small shift in the production (­increase/decrease), fb loop, or tumor → will get big exaggerated effects
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8
Q

What is grave’s disease?

A
  • Most common form of hyperthyroidism
  • Antibodies: thyroid stimulating (TSIs) globulins (autoimmune) - IgG
    • Bind with same receptors that bind to TSH
    • Bind on thyroid gland → causing overproduction of TH (T3/T4)
  • Induce continual activation of cAMP – (hypermetabolic state)
    • T3/T4 → eventually go back in short/long feedback loop to hypothalamus to stop producing TSH
  • Problem: TSI longer ½ life than TSH (12hrs vs 1 hr)
    • Though there is negative feedback loop → much longer binding (TSI override feedback) = longer activation of TG to make T3/T4
      • Levels:
        • ­ increase T3/T4
        • ¯decreaseTSH
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9
Q

Symptoms of hyperthyroidism?

A

Symptoms- hypermetabolic

  • Anxiety
  • Irritability
  • Difficulty sleeping
  • Fatigue
  • A rapid or irregular heartbeat (tachycardia)
    • lots of changes on EKG
  • A fine tremor of hands or fingers
  • An increase in perspiration
  • Sensitivity to heat
    • Heat intolerant
  • Weight loss, despite normal food intake (hypermetabolic)
    • Early: wt loss
    • Late: increase appetite
  • Brittle hair
  • Enlargement of thyroid gland (goiter)
  • Light menstrual periods

Frequent bowel movements – diarrhea

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10
Q

What is goiter?

A
  • ex- Toxic multinodular goiter
    • Need surgical management
  • > 50 years of age in US (due to adenomas or other goiters)
  • Extreme enlargement
  • Dysphagia (difficulty swallowing)
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11
Q

Treatment of hyperthyroidism?

A
  • Beta blockers- S & S relief
    • decrease hypermetabolic state (decreaseBP/HR)
    • Symptom management
  • Anti-thyroid meds-propylthiouracil (PTU)
    • Inhibits conversion of T4 to T3
  • Radioactive Iodine
    • Ex: for iodine producing CA/Adenoma
  • Surgery
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12
Q

What are causes of hypothyroidism?

A
  • Hashimoto disease
    • Autoimmune destruction of gland
      • T cell mediated (will further recruit B cells)/ type IV hypersensitivity
    • Causes thyroid inflammation (thyroiditis)
  • Lack of iodine
  • Idiopathic causes
    • Ex: lack of appropriate enzymes required for thyroid hormone production
      • Usually tends to be genetic—can cause creationism
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13
Q

Symptom of hypothyroidism?

A

Symptoms – (opposite of hyperthyroidism) (“hypofunctioning person”)

  • Increased sensitivity to cold
  • CV:
    • decrease CO, BP, HR, baroreceptor function
    • changes on EKG
  • Fatigue
  • Constipation
  • Pale, dry skin
  • A puffy face
  • Hoarse voice
  • Elevated blood cholesterol level – due to hypometabolism
  • Unexplained weight gain
  • Muscle aches, tenderness and stiffness
  • Pain, stiffness or swelling in joints
  • Muscle weakness
  • Heavier than normal menstrual periods
  • Depression
  • Mental retardation in infants or in utero (or creatinism)
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14
Q

Treatment hypothyroidism?

A
  • Levothyroxine
  • Iodine – in the case of Iodine deficiency
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15
Q

What is hashimoto’s thyroiditis?

A

Hashimoto thyroiditis Autoimmune response:

  • Thyroid-specific CD4+ helper T cells → induce both the cellular (CD8+ cytotoxic T cells) and the humoral (antibody-secreting mature B cells)
  • Response:
    • Cytotoxic T cells (sensitization) → increase ­ level of cytotoxic T cell
      • primarily responsible for the parenchymal destruction
    • B cells
      • secrete inhibitory anti-TSH receptor and other antibodies.
      • Antithyroid peroxidase activity causes plasma cells to produce antiTSH receptor antibody
        • TWO RESPONSES: together = destruction of cells (hashimotos)
  • The antithyroglobulin and antithyroid peroxidase antibodies are unlikely to contribute to pathogenesis but serve as useful serologic markers of disease.
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16
Q

What is myxdema?

A

more extreme form of hypothyroidism

  • Almost total lack of thyroid hormone
  • Increase in chondroitin and hyaluronic acid causing interstitial fluid to increase (around joints) → cause edema/stiffness/pain
    • Dangerous
    • Causes: edema, sore, stiff joints, pain
  • Why? Reasons not clear
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17
Q

What is typically the cause when both TSH and T3/T4 levels are elevated?

A
  • excess TSH production: thyroid responds appropriately w/ increased T3, T4
  • Causes:

pituitary adenoma secreting TSH

ectopic TSH production (e.g. lung cancer – SCC)

  • increase­ TSH/­increase T3/4 = coming from higher up (pituitary adenoma or ectopic TSH prod (SC lung CA)
    • feedback loop not working = ectopic or CA producing TSH
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18
Q

What is the ongoing disease process when TSH is elevated but T3/T4 levels decreased?

A
  • thyroid dysfunction:- enough TSH to stimulate thyroid gland but thyroid gland has undergone destruction d/t AI
  • TSH- elevated
  • T3/T4- decreased
    • ­ problem is thyroid dysfx
      • Wrong with TG or iodine deficiency
  • Causes:
    • Hashimoto’s thyroiditis (auto-antibodies against thyroid proteins, e.g. thyroglobulin, thyroperoxidase)
    • iodide deficiency
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19
Q

What are some causes for the the TSH level being decreased and T3/T4 level being elevated?

A
  • TSH- decreased
  • T3/T4- elevated (signal for T3/T4 coming from something other than the thyroid.
  • Examples:
    • thyroxine production not under control of TSH: usually under TSI (autoimmune)
    • Graves’ disease- immunoglobulin mimicking TSH function–> maintain negative feedback loop for decreasing TSH
    • toxic goiter
  • thyroxine secreting thyroid cancer
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20
Q

What are some cuarses for both TSH and T3/T4 levels being decreased?

A
  • TSH- decreased
  • T3/T4 - decreased
  • Cause: pituitary dysfunction: supratentorial dysfunction
    • Panhypopituitarism- no stimulation of having TSH
    • Null cell adenoma- bulk disturbance in pituitary gland → pressing on tissue preventing production/ release of TSH
    • Sheehan’s syndrome
      • Massive blood loss (r/t child birth or trauma)
      • lack of BF to brain (pituitary gland) → impact TSH production
        • one of the most sensitive areas- can lead to pituitary anoxia & dysfunction—leading to panhypopituitarism
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21
Q

What is cretinism?

A
  • Extreme hypothyroidism in fetal life, infancy or childhood
    • Lack of the gland ­– (genetic)
    • Lack of thyroid hormone – (genetic)
    • Lack of iodine – (most common)
      • Developing countries: Mom not get enough iodine or child not get enough in food after birth
  • Skeletal growth is more stunted than soft tissue
    • Disproportionate stunting of growth
    • Obesity, large tongue, etc
      • Skeletal bones smaller than soft tissue
      • *Malformed dwarf (versus well-formed dwarf d/t lack of GH)
  • PICTURE: characteristic facial features (flat, wide nose, large tongue), dwarfism (44 inches), absent axillary & scant pubic hair, poorly developed breasts, potbelly, & small umbilical hernia
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22
Q

What is the adrenal gland?

A
  • Adrenal glands are located on both sides of body in retroperitoneal, above and medial to kidneys.
  • Cortex with diff layers/ zones.
    • The Adrenal Cortex = produces hormones
      • Aldosterone
      • Cortisol
      • androgens
  • Zones:
    • zone glomerulosa- aldosterone
    • zona fasciulata- cortisol
    • zona reticularis- androgens
    • medulla- catecholamines
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23
Q

What is the zona glomerulosa?

A
  • Outermost
    • lies right under fibrous cap of the gland & produces aldosterone (a mineralocorticoid)
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24
Q

What is the zona fasiculata?

A
  • between glomerlosa & reticularis
    • Largest of the 3 layers (80% volume of cortex)
    • Responsible for glucocorticoids –
      • Ex: Cortisol
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25
Q

What is the zona reticularis?

A
  • Lies directly adjacent to medulla (innermost layer of adrenal cortex.)
    • Produces androgens – mainly DHEA and DHEA sulfate.
26
Q

What is the adrenal medulla?

A
  • Contain chromaffin cells of gland.
    • Main source of catecholamines – NE/Epi
      • NE: 20% of supply
      • Epi: 80% supply
        • Tumor → more NE produced
  • Arenal Medulla controlled by SNS via pregang fibers
    • Preganglionic fibers arise from T5 to T11.
    • Bc innervation from pregang nerve fibers → AM considered a specialized sympathetic ganglion.
    • But unlike other sympathetic ganglia, AM doesn’t have distinct synapses
      • Releases NE/Epi directly into blood supply
27
Q

What are corticosteroids?

A

Mineralocorticoids-

  • Aldosterone (rleased by zona glomerulosa)- Regulated by Ang II and extracellular K+
    • Kidneys- distal tubules and collecting ducts
    • ­increase Reabsorption of Na+ and excretion of K+ and H+
    • Control blood volume
      • Responsible for 2% of GFR
      • Influences BP & BV

Glucocorticoids-

  • Cortisol (released by zona fasciculata)- Regulated by CRH, and ACTH
    • Metabolism
    • Increase circulating glucose
      • Increase in mobilization of AA from protein
      • Stimulating synthesis of glucose from AA in liver (gluconeogenesis)
      • Increase level of FFA
        • Cells use to obtain energy
    • suppress immunity
      • anti-inflammatory effect: prescribe 5 day series of cortisol dexamethasone/solumedrol (asthma → decrease IgG response)
    • decrease Ca++ absorption by GI
28
Q

Catecholamies released by adrenal gland?

A
  • Epi (mostly), NE
  • Increase HR, BP
    • water soluble
    • catecholamine- structure made of catechol & amine group.
    • Adrenal glands responsible for most of adrenal that circulates in body.
    • NE
      • Adrenal gland- 20%
      • Neuroendocrine (brain)- 80%
29
Q

What is pheochromocytoma?

A
  • Pheochromocytoma- Neoplasm of chromaffin cells (cells in the adrenal medulla)
  • Catecholamine Secreting Tumors- tend to be hypermetabolic
    • Secrete mostly NE
      • 85:15 ratio to Epi
    • Very rarely (15% of tumors) Epinephrine predominates
      • Regular production: Epi > NE (80:20)
      • Secreting Tumor: Epi < NE (15:85)
        • Massive action alpha adrenergic receptors (BV- Alpha 1)
        • Massive vasoconstriction, tachycardia, arrythmias, F/F response from excess NE/Epi
30
Q

Symptoms of pheochromocytoma?

A
  • Rapid heart rate
  • Irregular heartbeat (palpitations)
  • Excessive sweating – intolerance to heat
  • Chest pain
  • Upper abdominal pain
  • Severe headaches – usually why they present first . Usually do a TSH test to determine if hyperthyroid/Graves’ disease
  • Shaking (tremors) of the hands
  • Feeling of anxiety
  • Feeling of extreme fright
  • Pale skin
  • High blood pressure
  • Orthostatic hypotension (decreased volume status)- constricted from the NE but tend to be depleted volume-wise
  • Tend to be young & very sick. Can cause strokes from htn
31
Q

Treatment for pheochromocytoma?

A
  • Alpha blockers
    • Block 1st- LONG ACTING (phenoxybenzamine) to VD
      • Why? Bc Know NE > Epi
      • AND Don’t want to BB before alpha or heart will fail
        • Taking away chronotropy and inotropy → cant pump against the vasoconstriction
  • Beta blockers 2nd
    • Reduce BP and optimize
  • Surgery- 3rd- usually come for surgery to ablate the tumors
    • Resecting tumor→ challenging
      • Overproduction of hormones while removing it
      • Massive response → Labile in OR
        • Causes strokes, Ortho HoTN (body not respond well to position and volume changes)
    • Intraoperatively- Be ready with Nipride when surgeon touches the tumor
32
Q

What are some adrenal cortex pathologies?

A
  • Adrenal Hyperfunction
    • Hypercorticalism (Cushing Syndrome/Disease)
      • Primary – pituitary tumor (last semester we learned this as cushing disease…)
        • sends too much ACTH for the adrenal gland to produce cortisol
      • Adrenal – adrenal tumor (last semster, we learned this as cushing syndrome…. unclear if this differentiation still exists…she did not cover this)
      • Paraneoplastic – ACTH secreting tumor outside pituitary
        • Small cell carcinoma (lungs)
      • Iatrogenic
    • Hyperaldosteronism (Conn’s Syndrome)
      • Primary – too much aldosterone
      • Secondary – dec BP or NA –> too much renin ® ↑ angiotensin ® ↑ aldosterone
  • Adrenal Hypofunction
    • Chronic Adrenocortical Insufficiency (Addison’s Disease)
33
Q

Causes of cushing’s syndrome? Effects of cushing’s syndrome?

A

Causes:

  • ACTH dependent – glucocorticoid excess
    • Most common: Cushing’s → Excess ACTH (ACTH dependent)
  • OR None dependent (ACTH independent)
    • Result of Prolong tx with glucocorticoids or underlying disease (HPA axis or production of cortisol)

Effects:

  • Increases blood glucose
  • Increases protein catabolism causing muscle wasting and weakness
    • (obese w/ a lot less musc & more fat mass)
  • Mobilization of fat from lower body to abdomen, face, trunk, back
    • (skinny legs with bigger bodies & hump back with a moon face)
34
Q

Symptoms of hypercorticalism? (cushing syndrome)

A
  • Weight gain, particularly around midsection and upper back
  • Fatigue
  • Muscle weakness
  • Rounding of face (moon face)
  • Facial flushing
  • Fatty pad or hump between shoulders (buffalo hump)
  • Pink or purple stretch marks (striae) on the skin of abdomen, thighs, breasts and arms
    • (progressive thinning of skin)
  • Thin and fragile skin that bruises easily
  • Slow healing of cuts, insect bites and infections
  • Depression, anxiety and irritability
  • Thicker or more visible body and facial hair (hirsutism)
  • Acne
  • Irregular or absent menstrual periods in females
  • Erectile dysfunction in males
  • High blood pressure
    • Edema in lower extremities → leading to HTN
  • ACTH dependent** → hyperpigmentation
35
Q

What is pituitary cushing syndrome, adrenal cushing syndrome, paraneoplastic cushing syndrome, and iatrogenic cushing syndrome?

Which ones are ACTH dependent? Which ones arent?

A

Schematic representation of various forms of Cushing syndrome. Illustrating the three endogenous forms as well as the more common exogenous (iatrogenic) form.

  • Primary: Pituitary Cushing Syndrome (most common)
    • Tumor in Anterior Pituitary gland → producing excess ACTH→ stimulates cortisol production
      • ACTH dependent
  • Adrenal Cushing Syndrome
    • Tumor in adrenal gland → producing excess cortisol
      • NonACTH dependent (independent)
  • Paraneoplastic Cushing Syndrome
    • Other types of tissues produce ACTH (Small cell carcinoma in lungs)
      • Ex: “Extra-Adrenal” → ACTH production → increase cortisol
      • ACTH dependent
  • Iatrogenic (Exogenous)
    • Take steroids → Cushing Syndrome (hyperglycemia, HTN)
      • Taper dose
      • NonACTH dependent
36
Q

Treatment for hypercorticalism?

A
  • Reducing corticosteroid use
    • Iatrogenic: If on steroids- try to taper
  • Surgery
    • Ablate tumor in gland itself
  • Radiation therapy
    • In pituitary gland
  • Medical therapy (drugs to block specific enzymes)
    • cortisol pathway has many enzymatic steps
37
Q

What is conn’s disease?

A
  • Primary Aldosteronism (hyperaldosteronism)
  • Caused by tumors in zona glomerulosa of adrenal gland
    • Excess Aldosterone
  • Sodium retention
  • Water retention
  • HTN
  • Leads to hypokalemia
  • Metabolic alkalosis (Hydrogen ion depletion)
  • Increases in ECF and blood volume → hypervolemic HTN
  • Conn’s Syndrome (same as conn’s disease)
    • Tumor in zona glomerulosa (aldosterone production) → impacts renal tubules and CD→
      • ­ increase Na Retention, total body Na, and ECF → leading to ­ increase BV & BP → ¯decreaseRenin production
        • increase ­ K & H+ ion excretion
        • Na escape phenomenon → further reduces [] K & becomes viscous circle of HTN
38
Q

What is addison’s disease?

A

adrenocotrical insufficiency

  • Caused by:
    • Primary atrophy of gland
      • Western worlds → tends to be more AI (primary atrophy)
        • D/t Ab against cells of AC
    • Injury to adrenal cortices (trauma- kidneys damaged, adrenal glands may be damaged)
      • Developing countries → d/t infections (TB)
  • Decreases mineralo- and gluco-corticoid hormones
    • pan decrease in both aldosterone & cortisol . primary hyoadrenalism
    • Aldosterone:
      • Depletion of ECF with decrease in Na, BP and CO; and hyperkalemia, mild acidosis
        • Opposite of Conn’s
    • CORTISOL
      • Ability to maintain blood glucose is diminished, as is mobilization of fat and proteins, decreasing metabolic function, and decreased ability to respond to stressors
        • (can’t respond to CV stress in particular) (opposite of Cushing’s disease)
39
Q

What is an adrenal crisis? Management?

A
  • Untreated Addison’s Disease: ADRENAL CRISIS
    • Extreme low levels of Glucocorticoid and mineralocorticoid → result in hypovolemic shock, vomiting, fever, stupor, coma
      • Management: hydrocortisone injections
40
Q

Symptoms of addison’s disease?

A
  • Muscle weakness and fatigue
  • Weight loss and decreased appetite
    • Darkening of the skin (hyperpigmentation)
      • especially on face
        • If not making cortisol –> high ACTH –> produce lots of cast offs from POMC, including MSH –> more skin pigment (tan tongue, nail bed, etc.)
  • Low blood pressure, even fainting
  • Salt craving
    • bc of hyponatremia
  • Low blood sugar (hypoglycemia)
    • pt unable to handle acute stress
  • Nausea, diarrhea or vomiting
  • Irritability
  • Depression
  • If extreme→ stupor & coma
41
Q

Treatment of addison’s disease?

A
  • HRT – corticosteroids
  • DHEA- androstenolone, etc.
    • (replace mineralocorticoids)
42
Q

Primary and secondary hyperparathyroidism?

A
  • Primary hyperparathyroidism
    • Excess secretion of PTH from one or more parathyroid glands
      • 4 glands total (due to the stimulating hormone)
    • usually caused by adenoma or hyperplasia (adenoma = 1 gland, hyperplasia = > 1 gland)
  • Secondary hyperparathyroidism
    • Increase in PTH secondary to a chronic disease
    • usually caused by low Ca++ or high phosphate
      • Signals to PT gland to produce more PTH → can cause feed forward mechanism w/ increasing PTH in response to low Ca levels
43
Q

What is hypoparathyroidism?

A
  • Abnormally low PTH levels
  • Usually caused by parathyroid damage in thyroid surgery (due to close proximity)
44
Q

Symptoms of hyperparathyroidism?

A
  • Hypercalcemia, Hypercalciuria
  • Kidney stones ***
  • Heartburn or abdominal pain
    • from peptic ulcer disease or pancreatitis
  • Nausea, vomiting or loss of appetite
  • Thinning bones (osteoporosis), leading to an increased risk of fractures
    • Mobilization of Ca from bones
  • Confusion or poor memory
  • Muscle weakness or fatigue , seizures
45
Q

Treatment for hyperparathyroidism?

A
  • Surgery – cannot remove all four parathyroid glands permanently
    • One placed back into body (Ex: forearm)
46
Q

Causes of hypoparathyroidism? Implications?

A
  • Caused by
    • Removal or trauma
    • Genetic disorders
    • Autoimmune
  • Decreases calcium levels
  • Osteoclasts become almost totally inactive
47
Q

Symptoms hypoparathyroidism? Treatment?

A
  • Paresthesia in the hands and feet
    • d/t alterations in nerve firing
  • Fatigue
  • Headaches
  • Bone pain
  • Insomnia
  • Tetany:
    • Spasms in smaller muscles
      • Ex: hand, feet, larynx (fingers, toes) à r/f laryngospasm
    • Low ionized calcium levels in the ECF increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials in small muscles = muscle spasm
  • Tx: PTH and Vitamin D
48
Q

How is the pituitary gland divided?

A
  • Anterior
  • Posterior
  • Intermediate: avascular in humans (prominent in other species)
49
Q

Cell types in anterior pituitary?

A
  • Somatotrophs: produce human GH
    • 30-40% of cells that make up anterior portion
  • Corticotrophs – produce ACTH (adrenocorticotropin)
    • 20% of cells
  • Thyrotrophs – TSH
  • Gonadotrophs – LH & FSH
  • Lactotrophs - Prolactin
    • Each of these 3-5% of cells of AP
50
Q

What is produced in posterior pituitary gland?

A
  • Nerves come directly from Hypothalamus.
    • These hormones are synthesized by cell bodies in HT.
      • ADH- affect on Kidneys
      • Oxytocin
51
Q

What are some posterior pituitary syndromes?

A
  • Central Diabetes Insipidus
    • Inability to concentrate urine
    • Polyuria, polydipsia, and dehydration
  • SIADH – Syndrome of Inappropriate ADH – FVE
    • Increase of ADH → retention of fluid
  • Oxytocin deficiencies –
    • few symptoms bc only req at child birth and breast feeding
      • studies recently (mostly w/ adult males) w/ lack of oxytocin
        • hard time bonding w/ mom
52
Q

Causes of hypopituitarism?

A
  • Null cell adenoma
    • not producing anything
      • bulk disorders → starts growing, don’t realize as soon bc no other symptoms until so large it compresses the optic chiasm or suppresses hormone production
  • Ischemic necrosis/Sheehan syndrome
    • decrease of BF to brain from trauma or childbirth
  • Ablation
    • cut out anterior pituitary when have adenoma → decrease in all anterior hormones
53
Q

Hyperpituitarism and pituitary adenomas types?

A
  • Prolactinomas
  • Growth hormone adenoma
  • ACTH adenoma
  • Gonadotroph cell adenoma
  • TSH cell adenoma
54
Q

What is diabetes insipidus?

A
  • Insufficiency of ADH
    • Polyuria and polydipsia, dehydration
  • Partial or total inability to concentrate the urine
    • urine hypo-osmotic
    • blood hyper osmotic
  • Neurogenic
    • Insufficient amounts of ADH (in pituitary gland)
      • hyperosmotic blood. Supplemental ADH will help
  • Nephrogenic (secondary mechanism)
    • Inadequate response to ADH in the kidney (end organ problem/not responsive)
      • not strictly a posterior pituitary problem → similar clinical presentation as central.
      • Supplemental ADH wont help these pts
55
Q

What is SIADH?

A
  • Hypersecretion of ADH- Syndrome of inappropraite ADH
  • Clinical manifestations are related to:
    • Enhanced renal water retention
    • hyponatremia
    • hypoosmolarity of blood
      • Causes → seizures, coma, brain swelling
  • For diagnosis normal adrenal and thyroid function must exist
  • Clinical manifestation are related to enhanced renal water retention, hyponatremia, and hypoosmolarity (blood becomes more dilute) (290 v. 250)
    • rapid fall in plasma osmolarity –> cell swelling
    • Big problem = neuronal swelling (they are inside skull that doesn’t expand) –> coma and death
  • Urine is hyperosmotic
  • Blood is dilute, urine is concentrated = too much ADH
  • Blood dilute, urine is dilute = water intoxication (too much water) not SIADH
  • Often seen in “slow” marathon running drinking too much water
    • Treatment – IV hypertonic saline administered “slowly”
  • Can also be seen with ADH secreting tumors
    • Treatment – remove the tumor – don’t bother to try to correct plasma osmolarity
56
Q

What are some causes of hypopituitarism?

A
  • Pituitary infarction
    • Sheehan syndrome- necrosis due to heavy blood loss in delivery of baby.
      • During pregnancy → pituitary enlarged & more susceptible to ischemia
    • Hemorrhage
    • Shock
      • Decrease in ALL AP hormones, PP will be unaffected by ischemia (if its not from trauma- damage to pituitary stalk will affect posterior)
  • Panhypopituitarism: usually due to cell destroying tumors (drop in ALL hormones)
    • ACTH deficiency
    • TSH deficiency
    • FSH and LH deficiency
    • GH deficiency
      • Will be sick (symptoms from lack of ALL hormones)
57
Q

Causes and manifestations of hyperpituitarism?

A
  • Commonly due to a benign, slow-growing pituitary adenoma (goes undetected due to slow growth)
    • Tumors can become HUGE
    • Transphenoidal approach to remove (watch for CSF leaks)
  • Manifestations:
    • Headache and fatigue
    • Visual changes – B/L temporal hemianopsia, loss of peripheral vision
    • Hyposecretion of neighboring anterior pituitary hormones (due to bulk disturbances)
      • Depending on tumor location → will press and cause a decrease in hormone secretion
58
Q

What is a pituitary adenoma?

A
  • Massive, nonfunctional adenoma has grown far beyond the confines of the Sella turcica and has distorted the overlying brain. Nonfunctional adenomas tend to be larger at the time of diagnosis than those that secrete a hormone.
    • Slow growing → continue for so long
    • Symptoms gradual (until blurred vision→ blindness)
59
Q

What happens to pituitary cells when an adenoma is present?

A

The monomorphism of these cells contrasts markedly to the mixture of cells seen in the normal anterior pituitary.

  • Monomorphism- one type of cell overgrowing
    • Overgrowth in one type of cell
    • Hypogrowth in other types of cell (other type of cell is decreasing)
      • Somatotrophs (GH): 30-40%
      • Corticotropes (ACTH): 20%
      • Thyrotropes – TSH (5%)
      • Gonadotrophs – LH & FSH (5%)
      • Lactotrophs- Prolactin (5%)
        • Prominence of that type of cell versus deficiency in others
60
Q

What is acromegaly vs gigantism?

A

Hypersecretion of Growth Hormone (GH) – growth factor for connective tissue

  • Acromegaly (long bones grow through apposition)
    • Hypersecretion of GH during adulthood
    • Thickening of skin on scalp
    • Large forehead/head, forward projection of jaw, & protrusion of frontal bone
      • **overgrowth of soft tissue
      • Prolonged GH excess → *Develop DMII, reduced sexual function
  • Gigantism (very tall due to skeletal muscle increase)
    • Hypersecretion of GH in children and adolescents
    • Excessive secretion of growth hormone by the anterior lobe of the pituitary gland during the early years of life produces giants of this type, whereas deficient secretion of this substance produces well-formed dwarfs.
      • **Overgrowth of skeletal bones
    • GH = anabolic effect (building up)
    • Like other protein hormones → act w/ receptors a
      • receptors are increasing in height in child and adolescents, increase in muscle mass, lipolysis, protein synthesis, etc.
61
Q

What is dwarfism?

A
  • Lack of GH
    • Primary Deficiency: Alterations in somatomedin that results in GH deficiency
    • Secondary: failure of tissues to respond to somatomedin or failure of liver to produce somatomedin.
  • Generalized deficiency in childhood
  • Stunts growth
  • Body develops appropriately proportional- rate is slowed down
    • Skeletal and muscular system tend to form together= well-formed dwarf
    • Normal face, head, trunk, & limbs of approximately normal proportions vs cretinism à disproportional growth
  • Inability to go through puberty- delayed
    • In 1/3rd → only GH is missing/reduced (can develop sexually and reproduce)
    • Tends to lead to→ sexual dysfunction, delayed puberty/sexual fx
  • Rare in adults
    • most common from pituitary adenoma
      • Might see idiopathic growth that’s not occurring or bc of trauma
62
Q

Summary of all endocrine disorders.

Grave’s disease?

hashimoto’s?

Cretinism?

Cushings?

Conns?

Addisons?

Sheehans?

Acromegaly?

Gigantism?

A

Graves – Hyperthyroidism

Hashimoto’s – Hypothyroidism

Cretinism – Hypothyroidism in fetal life

Cushing’s – Hypercortisol

Conns – Hyperaldosteronism

Addison’s –adrenocortico insufficiency (aldosterone/cortisol)

Sheehan’s – Hypopituitary (due to insult/¯blood flow to pituitary)

Acromegaly – Increased growth hormone in adulthood

Gigantism – Increased growth hormone in children

Patho Test 4 (4 decks)

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