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Patho > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Why is Endocrine System Important

A
  • Growth and development
  • Response to stress and injury
  • Reproduction
  • Regulation of energy metabolism
  • Ionic hemostasis
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2
Q

What is the Biologically Critical Ions

A

Sodium (NA): 135 -145 mEq/L
Potassium (K): 3.5 - 5.0 mEq/L
Cacium (Ca): 8.5 - 10.5 mg/dL
Magnesium (Mg): 1.5 - 2.5 mg/dL
- CO2 & HCO3 is also important

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3
Q

Why is Ionic Homestasis important?

A

A Proper ionic balance essential for muscle coordination, heart function, nerve function, fluid absorption and excretion (Blood Volume, Blood Pressure).
- Serum Osmolarity: 280-290 mOsmol/kg
- Serum pH: 7.35-7.45
- Outside this range cell, organs dysfunction and death occur

Ions conduct electricity and are found in body fluid, tissue, and blood
- Cell membrane potential
- CNS, CV, Epithelial cell polarization

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4
Q

Is every endocrine dysfunction caused by endocrine disorder

A

No it is not only caused by it.
- There can be other reasons too like diabeites

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5
Q

Endocrine Disease

A

Indolent Progression (grow slowly and doesn’t cause pain)

Hormone-secreting cells widely distributed in the body in all organs
- Non specific presentation
– Subclinical syndromes

Differential diagnosis is critical

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6
Q

Endocine Organs

A

Majority of them are EPITHELIAL
- Secretion hormones => Vascular organs (Ductless)
– It got a regulated release of products
- Ability to modulate activity: structure
- Variable storage reserve

Disease/Dysfunctions
- Under-activity / Over-activity
- Neoplasia
- Autoimmune disease (esp. vulnerable to it)

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7
Q

Endocrine Tissue Classification

A
  • Neuroendocrine system
  • Steroid hormone-secreting cells
  • Epithelium Thyroid
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8
Q

Neuroendocrine system

A

Origin:
- Epithelial (pituitary, Islet, endocrine cells, lung, gut)
- Endodermal
- Neuroecttoderm (adrenal medulla, paraganglia, thyroid parafollicular C cells, parathyroid gland)

Produce:
- Peptide hormones (many can function as neurotransmitters)

Characterized by
- Well-developed RER for peptide synthesis
- Large Glgi complexes for packaging
- Numerous SECRETORY GRANULES
– they store and transport hormones to the cell surface for release by exocytosis

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9
Q

Steroid Hormone-Secreting Cells

A

Arise from the mesodrem (adrenal cortex and steroidogenix cells of the testes and ovaries)

Produce:
- They take cholesterol and produce fat soluble hormones (glucocorticoids, mineralocorticoids, estrogens, testosterone and its precursors.)

Characterized by
- Well developed SER
- Large mitochondria (can metabolize cholesterol throught expression of side chain cleavage)

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10
Q

Thyroid Follicular Epithelium

A

‘unique’ epithelial cell type of endodermal origin

Synthesize and produce THYROID HORMONES

Characterized by
- Tight junction (needed for critical follicular structures that are the site of storage)
- Prominent microvilli (necessary for reabsorption of that substance for thyroid hormone synthesis)

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11
Q

What is a Hormone?

A

A chemical substance that can affect the tissues of the body

Water-Soluble Hormones (can’t get into the cell)
- bind to receptor (GPCRs) at the cell surface
- Triggers the activation and/or production of intracellular proteins/enzymes

Lipid-Soluble Hormones
- Hormone-receptor complex binds to a
specific site on the promoter region on DNA
- Activates RNA polymerase
- Stimulates DNA transcription
- Production of intracellular proteins/enzymes

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12
Q

Cellular Mechanisms of Hormone Actions

A

Target Cells:
- Express hormone receptor which bind to hormones
- Hormone-receptor binding initiates a signal to modulate cellular function

Sensitivity of a target cell to a homone can be Upregulated or Downregulated
- Receptor mutation (insensitivity)
- Hormone mutation (Gain of function, Loss of function, polymorphisms)

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13
Q

Hierarchical Control of Hormone Release

A

Hypothalamus (Release Hormones) ==> Anterior Pituitary (Stimulating Hormones) ==> Adrenal ==> Cell and tissues of the body

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14
Q

Posterior pituitary hormones

A

Antidiuretic Hormones (ADH)
Oxytocin

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15
Q

Anterior Pituitary Hormones

A
  • Growth hormone (GH)
  • Adrenocorticotropin (ACTH)
  • Thyroid-stimulating hormone (TSH)
  • Follicle stimulating hormone (FSH)
  • Luteinizing hormone (LH)
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16
Q

Antidiuretic Hormone

Water-soluble

A

Maintain blood pressure, blood volume and tissue water content by controlling the amount of water urinated

Major Stimuli
- Hyperosmolarity (↑POSM); sensed in hypothalamic nuclei
- Volume depletion; sensed by carotid baroreceptors

ADH co-produced and released with CRH (Corticotropin-releasing hormone)

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17
Q

ADH MOA

A

1) ADH attaches to V2 receptor
2) Activate cascade through Gs protein, adenylyl cyclase, cAMP, and PKA (protein kinase A)
3) Caused insertion of aquaporin 2 into apical membr
4) H2O moves through aquaporin 2 in response to osmotic gradient and go into the basolateral membrane

This result in increasing Blood Volume and decreasing Urine Volume
Receptors are located in the Collecting ducts of the kidney

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18
Q

Dysfunction of the Posterior Pituitary

Hypofunction

A

Hypofunction:
- Diabetes Insipidus ( deficiency in ADH)

Etiology (cause):
- Neurogenic
- Nephrogenic
- Psychogenic
- Drug-induced
- Inability to concentrate Urine
- Decreased water reabsoption in kidney
– Decreased Blood Volume, Pressure
– Increased serum electrolytes (Na+: thirst, tachycardia, lethargy, dehydration, thirst, tachycardia, lethargy, dehydration, disorientation, weakness, irritability, muscle twitching)

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19
Q

Dysfunction of the Posterior Pituitary

Hyperfunction

A

Hyperfunction
- Syndrome of inappropriate ADH secretion (SIADH)

Etiology (cause)
- Neoplasms
- Surgery
- Disease States
- Psychiatric
- Drug-induced

Pathophysiology of SIADH
- ADH continuously released,
– BP, BV increase- BP, BV increase
Hyponatremia (lethargy and confusionlethargy and confusion)

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20
Q

Dysfunction of the Anterior Pituitary

Hypofunction

A

Hypopituitarism
- Cortisol Deficiency (ACTH), Thyroid deficiency (TSH), Gonadal failure, Loss of 2 sex characteristics(LH, FSH), growth deficiency (GH)

Etiology:
- Primary: Intrinsic pituitary disease
- Secondary: Hypothalamic disorders
- Functional: Anorexia, Chronic starvation

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21
Q

Pathophysiology of Anterior Pituitary
hypofunction

A

TSH deficiency: Loss of Thyroid hormone production
LH, FSH deficiency
GH deficiency GH deficiency
ACTH deficiency: Loss of adrenal hormone production
- Life threatening; need to immediately intervine

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22
Q

If Brain Injury Patient

A

You should make a G,T,A study
- To make sure everything is okay and intervine right away

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22
Q

Dysfunction of the Anterior Pituitary

Hyperfunction

A

Hyperpituitarism
Etiology:
- Pituitary adenoma (secretory)

Pathophysiology: Compression Brain injury
- Hypersecretion of Anterior Pituitary hormones
– Prolactin Prolactin
– GH- GH
– ACTH

23
Q

Acromegaly

A
  • Decreased life expectancy
  • Cardiovascular disease
  • Diabetes
  • Arthropathy
  • Neuropathy
24
Q

Thyroid gland

A

Thyroxine (T4) and triiodothyronine (T3):
- Key regulators of metabolism and development and are known to have pleiotropic effects in many different organs
– Increase level of body metabolism
– Regulator of cardiovascular functions
- T4 is the major product
- T3 is most potent/best measure of hyperthyroidism

Calcitonin
- Promotes deposition of calcium in the bones (decreases circulating Ca++)

25
Q

Changes in cardiovascular hemodynamics is associated with thyroid dysfunction

A

Check Screen Shot

26
Q

Alterations of Thyroid Function

A

Hyperthyroid Conditions
- Graves Disease
- Diffuse toxic goiter
- Drug-induced: excess L-thyroxine administration

Hypothyroid Conditions
- Hypothyroidism
– Primary
– Secondary
- Thyroiditis
– Autoimmune (Hashimoto disease)
– Acute, subacute

27
Q

Goiter

A

Can be
- Hyperthyroid
- Euthyroid
-Hypothyroid

28
Q

Graves’ Disease

A

Hyperthyroidism; Associated with thyroid enlargement
- Familial disorder
- Occur in youn females (20-40)
- M:1 = 1:7
- Ocular changes with exophthalmos
- Pretibial edema of legs
- Auto-immune etiology
– Stimulatory Thyroid receptor antibodies
- Elevated T4, T3 and depressed TSH

Most common cause of endogenous Most common cause of endogenous hyperthyroidism

check screen shot

29
Q

Diffuse Toxic Goiter

A

Induced by stressor
- Irreversible change to follicular cells
- Autonomous function (no feedback control)
– Involution of remaining gland
— Toxic Multinodular goiter

Similar to Graves disease
- but no opthalmopathy, pretibial myxedema

30
Q

Thyrotoxic crisis

A

Untreated hyperthyroidism:
- Acute Stressor
– Hyperthermia
– Tachycardia
– Heart failure
– Delirium
– N/V/D
- Chronic untreated effects

High T4/T3 is associated with low TSH (negative feedback)

31
Q

Hypothyroidism

A

Primary
- Loss of thyroid tissue (autoimmune)
- Chronic lymphocytic thyroiditis/Hashimoto’s Thyroiditis

Secondary
- Pituitary, hypothalamus disease
- Peripheral resistance to T3/T4

32
Q

The Major change that happen with Hypothyroidism

A

The major cardiovascular changes that occur in
hypothyroidism include a decrease in cardiac output and cardiac contractility, a reduction in heart rate, and an increase in peripheral vascular resistance

33
Q

Hashimoto’s Thyroiditis
(Chronic Lymphocytic Thyroiditis)

A
  • Painless swelling
  • In middle aged females (45-65)
  • F:M = >10:1
  • Caused by TSH-receptor auto antibodies
  • Result in gradual onset of hypothyroidism
34
Q

Hypothyrodism Vs Hyperthyroidism

A

Screen Shot

35
Q

DeQuervain disease

A
  • Granulomatous thyroiditis (subacute)
  • Patients may initially be hyperthyroid, then Patients may initially be hyperthyroid, then euthyroid.

Prior viral infection has been implicated

36
Q

Pathophysiologic consequence of chronic dysthyroid states

A

Cardiovascular disease
- Hyperthyroid states: Atrial Fibrillation (AF), cand it’s cardiovascular Disease
- Hypothyroid states: ↑ cholesterol, Hypertension, atherosclerosis

Thyroid hormone excess on bone metabolism
- Higher osteoporosis risk in people with overt and subclinical thyrotoxicosis.

CNS effect
- Fetal neurodevelopment, neuropsychiatric morbidit (adult)

Thyroid dysfunction and its previous treatment have been implicated in the development of cancers
- Potential carcinogenic effect of radioiodine therapy in the treatment of hyperthyroidism.

37
Q

Thyroid nodules

A

Very Common (8% population)
- Increase in incidence with age
- 50% of patients are over 50
- 95% are benign

38
Q

Thyroid Cancer

A

Most common endocrine related cancer
- 3.6% of all new diagnosed cancer in U.S
- 60% of thyroid cancer are diagnosed while cancer in primary site
- 25% diagnosed after spread to regional lymph (beyond primary site)
- 5% are diagnosed after cancer metastasized

The incidence of thyroid cancer in females is > 3 times that of males
- Delay in primary treatment Increase probability of thyroid cancer death 2.4 fold

39
Q

When should one use ultrasound (US) and fine needle aspiration (FNA) in thyroid nodule evaluation?

Assessment of Thyroid Nodules

A

US examination indicated if a nodule or goiter is palpable and In patients WITHOUT palpable lesions who are at high rish of thyroid cancer
- FNA BIOPSY recognized as Diagnostic procedure of choice (clinically or incidentally discovered thyroid nodules)

40
Q

Which laboratory evaluations should be performed for thyroid nodules?

A

If there is no specific clinical suspect; The initial thyroid laboratory evaluation requires the determinatin of TSH ONLY
- Serum Calcitonin (MTC)

41
Q

Thyroid Cancer

A

Adenoma (up to 50% of solitary neoplastic nodules)
Carcinoma most common endocrine malignancy
- Papillary adenocarcinoma (65%)
- Follicular Carcinoma (25%)
- Medullary carcinoma- parafollicular cell (MTC; 5-10%)
– Originates from the parafollicular C (calcitonin producing) cells
- Anaplastic carcinoma (10-15%):
– Exxtremely poor prognosis: lethal
– fine needle aspiration biopsy of the mass shows malignant spindle-shaped cells that demonstrate a p53 mutation

42
Q

Chharacteristics of Papillary Thyroid Cancer

A

Peak onset 30-50: 3:1 (F:M)
- Prognosis related to tumor size
- 85% of thyroid cancer from radiation
- Metastasis to neck lymph nodes
- Distant spread is uncommon
- Cure rate is high

43
Q

Characteristics of Follicular Thyroid Cancer

A

Peak onset 40-69: 3:1 (F:M)
- Prognosis is related to tumor size
- Spread to lymph nodes is uncommon
- VASCULAR invasion is Common
- Cure rate is high in young: lower with higher age

44
Q

Adrenals

A

Outer Cortex:
Aldosterone (Mineralocorticoids)
- Sodium and fluid retention, resulting in ↑ in intravascular volume.
- Produced in Zona glomerulosa

Cortisol (Glucocorticoids)
- Multiple metabolic functions for the control of protein, carbohydrate, fat metabolism
- Produced in the Zone Fascicularis

Sex Androgens:
- Produced in the Zona Reticularis

Inner Medulla:
Norepinephrine/Epinephrine/Dopamine
- Increase BP, CNS Stimulation

45
Q

Cushining’s Syndrome

A

Adrenal Hyperfunction:
- Central Obesity (rapid weight gain to the face, neck and trunk, but sparing the extremities)
– Associated with kyphosis, amenorrhea or impotence, hypertension, and extreme weakness
- Hyperglycemia
- Hypertension
- Continued presence of Cortisol levels (promotes obesity)
- Ecchymoses
- Thinner hair
- Moon face, and ruddy complexion
- Mood swings

46
Q

Pituitary Tumors

A

Most common
- Increased serum ACTH (pituitary tumor) => Increased cortisol (enlarged adrenal cortex)
- Feedback infeffective

47
Q

Adrenal Cortex Tumor

A

Increased Serum Cortisol => Inhibit ACTH secretion (through feedback to the pituitary)
- THis mean we will have an increase in Cortisol and a decrease in the ACTH

48
Q

Paraneoplastic Syndrome

A

Increased serum ACTH and cortisol
- Lung Cancer (increased ACTH seccretion) => Enlarged Adrenal cortex => Increased cortisol secretion

49
Q

Iatrogenic

A

Increased Cortisol and decreased ACTH
Ingest Cortisol medication => Inhibit hypothalamic pituitary ACTH secretion => Adrenal Cortex atrophy => NO CORTISOL SECRETION

50
Q

Addisons Disease

Primary hypocortisolism

A

Increase in ACTH with inadequate corticosteroid synthesis
- diopathic organ-specific autoimmune etiology
– Destruction of adrenals: tuberculosis, trauma, etc.
- Women 30-60 years of age

Clincal Signs
- Weakness, N/V, GI disturbances, Hyperpigmentation
- Hypoglycemia-decr. Gluconeogenesis
- Recall CRH is CO-SECRETED with ADH: feedback control (Hyponatremia)

51
Q

Addisons Disease

Waterhouse-Friderichsen syndrome

A

Meningococcemia: Acute infection with Neisseria meningitidis can produce can produce this form of acute adrenal failure
- Petecbial rash, coagulopathy, Cardiovascular collapse, Bilateral adrenal hemorrhage
- Cases of purpura fulminans, cutaneous ecchymosis, hypotension, and fever in patients for whom the culture data are unknown classified as probable
meningococcemia.

52
Q

Adrenals-Aldosterone

Aldosterone

A

Deficiency: Hypoaldosteronism
- Hyperkalemia (high K+)
– Signs: abdominal cramping, fatigue, lethargy, and muscle weakness
– Sever Hyperkalemia will slow cardiac impulse conduction producing classic ECG changes
- Hypotension (low BP)

Excess: Conn’s syndrome
- Hypertension, Hypokalemia
- Resistant Hypertension

53
Q

Aldosterone

Mech: Excess

A

Binding of aldosterrone receptor to mineralcoricoid response element
- Increase transcription of gene encoding aldosterone inducible proteins
– Apica epithelial sodium channel (ENaC)
– Basolateral sodium potassium (Na/K) ATPase

This stimulate sodium (NA+) reabsorption and potassium (K+) excretion
- Hypokalemia, Hypertension

54
Q

Resistant Hypertension

A

Blood pressure that remain higher than normal despite the use of 3 antihypertensive medication
- They are at disproportionately high risk for target organ damage and cardiovascular events
- Associated with: Older age, more sever hypertention, chronic kidney disease, femal sex, black race, obesity, and diabetes

Recent studies indicate that primary aldosteronism is a common caus eof resistant hypertensio (2-20% prevalence)

55
Q

Challenges in Endocrine Pathophysiology

A

Early detection
Sensitive and specific accessible biomarkers
Coordinated multidisciplinary endocrine pathophysiology health care delivery support
Suspected Increasing incidence of endocrine diseases
- Neoplastic, Autoimmune, Drug-induced

Familial/genetic relationship
- Monogenetic/polygenetic: in dysfunction and neoplastic disease progression
- Morphology-genotype correlation

Patho (17 decks)

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