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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
Thyroid gland
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
Changes in cardiovascular hemodynamics is associated with thyroid dysfunction
Check Screen Shot
26
Alterations of Thyroid Function
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
Goiter
Can be - Hyperthyroid - Euthyroid -Hypothyroid
28
Graves’ Disease
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
Diffuse Toxic Goiter
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
Thyrotoxic crisis
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
Hypothyroidism
Primary - Loss of thyroid tissue (autoimmune) - Chronic lymphocytic thyroiditis/Hashimoto’s Thyroiditis Secondary - Pituitary, hypothalamus disease - Peripheral resistance to T3/T4
32
The Major change that happen with Hypothyroidism
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
Hashimoto’s Thyroiditis (Chronic Lymphocytic Thyroiditis)
- 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
Hypothyrodism Vs Hyperthyroidism
Screen Shot
35
DeQuervain disease
- Granulomatous thyroiditis (subacute) - Patients may initially be hyperthyroid, then Patients may initially be hyperthyroid, then euthyroid. Prior viral infection has been implicated
36
Pathophysiologic consequence of chronic dysthyroid states
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
Thyroid nodules
Very Common (8% population) - Increase in incidence with age - 50% of patients are over 50 - 95% are benign
38
Thyroid Cancer
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
When should one use ultrasound (US) and fine needle aspiration (FNA) in thyroid nodule evaluation? | Assessment of Thyroid Nodules
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
Which laboratory evaluations should be performed for thyroid nodules?
If there is no specific clinical suspect; The initial thyroid laboratory evaluation requires the determinatin of TSH ONLY - Serum Calcitonin (MTC)
41
Thyroid Cancer
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
Chharacteristics of Papillary Thyroid Cancer
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
Characteristics of Follicular Thyroid Cancer
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
Adrenals
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
Cushining's Syndrome
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
Pituitary Tumors
Most common - Increased serum ACTH (pituitary tumor) => Increased cortisol (enlarged adrenal cortex) - Feedback infeffective
47
Adrenal Cortex Tumor
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
Paraneoplastic Syndrome
Increased serum ACTH and cortisol - Lung Cancer (increased ACTH seccretion) => Enlarged Adrenal cortex => Increased cortisol secretion
49
Iatrogenic
Increased Cortisol and decreased ACTH Ingest Cortisol medication => Inhibit hypothalamic pituitary ACTH secretion => Adrenal Cortex atrophy => NO CORTISOL SECRETION
50
Addisons Disease | Primary hypocortisolism
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
Addisons Disease | Waterhouse-Friderichsen syndrome
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
Adrenals-Aldosterone | Aldosterone
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
Aldosterone | Mech: Excess
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
Resistant Hypertension
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
Challenges in Endocrine Pathophysiology
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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