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pathophys > M7: Endo, obesity, nutrition > Flashcards

M7: Endo, obesity, nutrition Flashcards

1
Q

Graves Disease

A

1 cause of hypothryorid (1.5-2%of females)

autoimmune disease-dev. antibodies
stimulation of the thyroid by autoantibodies directed against the tsh receptor. autoantibodies (thyroid-stimulating immunoglobulins or thyroid stimulating antibodies override the normal regulatory mechanisms.

7x more common in females

DX: radioactive reuptake test
Diffuse reuptake=graves
focal point area-not graves

CM: Exophthalmos: (incr secretion of hyalurinoic acid, orbital fat accum, inflamm, and edema of orbital contents
Pretibial myxedema: dermopathy: thickness/pigment changes, LE edema
TX: antithyroid meds, radioactive iodine, surg. tx: does not reverse infiltrative opthalmopathy or pretibial myxedema

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2
Q

Graves DS (2)

A

-TSI stimulation of tsh receptors in the gland results in hyperplasia of the gland (goiter) and increased synthesis of TH especially of T3. increased levels of TH result in classic signs and symptoms of hyperthyroidism.

TSH production in pitutiary inhibited through norm neg. feedback loop

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3
Q

Diabetes Insipidus-
ds of posterior pituitary

A

-Insufficient ADH activity leads to polyuria and polydipsia.
3 forms: neurogenic or central di, nephrogenic di, primary polydipsia or excessive thirst appreciation.

neurogenic or central DI- insufficient secretion of ADH.
-Occurs when any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release.
-Causative lesions include primary brain tumors, TBI, hypophysectomy, aneurysms, thrombosis, infections, and immunological disorders. Genetics.

nephrogenic DI- inadequate response of the renal tubules to ADH.
-caused by disorders and drugs that damage the renal tubules.
-Can include pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease. -Drugs can affect include lithium, colchicine, amphotericin B, loop diuretics, and general anesthesia. Genetics.

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4
Q

Diabetes Insipidus-Primary Polydipsia
ds of posterior pituitary

A

Primary Polydipsia- rare form of DI-
level of vasopressin-degrading enzyme vasopressinase is increased, resulting in ADH deficiency.

-have a partial to total inability to concentrate urine.
causes large volumes of dilute urine excretion, leading to increased plasma osmolality.

In conscious individuals, the thirst mechanism is stimulated and induces polydipsia; dehydration develops rapidly without ongoing fluid replacement.

-if the individual with di cannot conserve as much water as is lost in the urine, serum hypernatremia and hyperosmolality occur.

Concentrations of other serum electrolytes are generally not affected. Urine output can increase from a normal of 1-2 l/day to 8-12 l a day.

DX; includes polyuria, polydipsia, low urine specific gravity under 1.010, low urine osmolality, hypernatremia, high serum osmolality, and continued diuresis despite a serum sodium level of 145 or greater.

TX: based on the extent of adh deficiency. fluid replacement using oral, or iv routes is adequate. some people require adh replacement with the synthetic vasopressin analog desmopressin (DDVAP)

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5
Q

Cortisol

A

Stim-ACTH in the adrenal cortex; synthesized from cholesterol, lipid-soluble

Secretion is regulated primarily by the hypothalamus and anterior pituitary gland.

Most POTENT naturally occurring glucocorticoid

needed to maintain life and protect body from stress
-3 factors appear to be primarily involved in regulating the secretion of ACTH: negative feedback effects of high circulating levels of cortisol, diurnal rhythms with peak levels during sleep, and psychological and physiologic stress increase ACTH secretion, leading to increased cortisol levels.

  • Functions: Regulates blood sugar, reduces inflammation, controls blood pressure.
  • Dysfunction:
    Excess cortisol can lead to Cushing’s syndrome; deficiency may result in Addison’s disease.

Chronic steriod use-they have NO Cortisol, be very careful w/ tapering

Aging: clearance of cortisol is decr

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6
Q

Action of Catecholamines (epinepherine and norepinepherine)

A

Chromaffin cells AKA: pheochromocytes of the adrenal medula secrete epi/norepi; synth from the amino acid PHENYLALANINE
releasing into
FIGHT or FLIGHT mode/Sympathetic
(htn, tachy/arrhymias, vasoconstriction)

EX: adrenal medulla hyperfxn–
PHEOCHROOCYTOMAS

Promote hyperglycemia through interference with the usual glucose regulatory feedback mechanisms.

Clinical Significance: Imbalances can affect stress response, metabolic processes, and cardiovascular health.

Present in BAT (Brown Adipose Tissue) when exposed to cold-activates sympathetic rxn
T3 stim BAT to rapidly generate heat through activation of uncoupling protein 1 (UCP1)=
NON-SHIVERING THERMOGENESIS

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7
Q

Glands - Thyroid verus Parathyroid

A
  • Thyroid Gland: Produces thyroid hormones (T3 and T4) which regulate metabolism. (90/10 ratio)
  • parafollicular cells (C cells) secrete calcitonin, which decr CA++ levels
  • Parathyroid Gland: Produces parathyroid hormone (PTH) which regulates calcium levels in the blood.
  • Dysfunction:
    Hyper-/hypothyroidism affects metabolism, while hyper-/hypoparathyroidism impacts calcium balance.
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8
Q

Pancrease gland

A

Endocrine: produces hormones
Exocrine: digestive enzymes
Houses the Islets of Langerhans
Alpha=glucagon
B=insulin and amylin
D=somatostatin and gastrin

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9
Q

Acromegaly vs Giantism

A
  • Acromegaly: Caused by excess growth hormone (GH) in adulthood, leading to bone thickening and tissue growth.
  • Giantism: Occurs in children due to excess GH, resulting in abnormal height and growth.
  • Diagnostics: GH and IGF-1 levels, oral glucose tolerance test.
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10
Q

Hormone release

A
  • Mechanism: Typically regulated by the hypothalamic-pituitary axis via releasing and inhibiting hormones.
  • Significance: Ensures precise control of hormone levels, affecting growth, metabolism, and homeostasis.
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11
Q

Prolactin vs LH vs FSH

A
  • Prolactin: Stimulates milk production postpartum.
  • LH (Luteinizing Hormone): Triggers ovulation and testosterone synthesis.
  • FSH (Follicle-Stimulating Hormone): Stimulates ovarian follicle growth in females and spermatogenesis in males.
  • Regulation: Controlled by gonadotropin-releasing hormone (GnRH) from the hypothalamus.
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12
Q

Leptin, Adipocytes

A
  • Leptin: A hormone produced by adipocytes (fat cells) that helps to regulate energy balance by inhibiting hunger.
  • Significance: Leptin resistance can contribute to obesity and metabolic disorders.
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13
Q

Obesity including complications and risk assessment

A
  • Complications: Increased risk of type 2 diabetes, cardiovascular disease, certain cancers, and musculoskeletal disorders.
  • Risk Assessment: BMI measurement, waist circumference, family history, and lifestyle factors.
  • Management: Lifestyle modification, medication, possibly surgery.

**

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14
Q

Anorexia of aging

A
  • Description: Decreased appetite and food intake in older adults, leading to weight loss and nutritional deficiencies.
  • Etiology: Could be related to reduced sense of smell and taste, dental issues, medications, or social factors.
  • Clinical Significance: Increases risk of frailty, immune dysfunction, and poor quality of life.
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15
Q

GH and Insulin structures (are they steroids, amines, peptides? etc.)

A
  • Growth Hormone (GH): A peptide hormone that stimulates growth, cell reproduction, and regeneration.
  • Insulin: Also a peptide hormone; regulates metabolism by promoting the absorption of glucose from the blood.
  • Classification: Neither are steroids or amines; both are peptide hormones with complex protein structures.
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16
Q

Type 1 DM

A

Etiology: Autoimmune destruction of pancreatic beta cells.
Pathophysiology: Insulin production is severely impaired or absent.
Manifestations: Polyuria, polydipsia, weight loss, fatigue.
Diagnostics: Blood glucose levels, HbA1c, autoantibody testing.
Clinical Course: Lifelong insulin dependency, risk of ketoacidosis.
Other: Emphasis on lifelong management with insulin and lifestyle modifications.

17
Q

Type 2 DM

A
  1. Etiology: Genetic predisposition and lifestyle factors (obesity, minimal exercise).
  2. Pathophysiology: Insulin resistance and beta-cell dysfunction.
  3. Manifestations: Often asymptomatic initially, possibly similar symptoms to Type 1 diabetes when advanced.
  4. Diagnostics: Blood glucose levels, HbA1c.
  5. Clinical Course: Progressive; may be managed with lifestyle changes, oral medications, or insulin.
  6. Other: Focus on prevention through weight management and regular exercise.
18
Q

DKA

A
  1. Etiology: Predominantly in Type 1 diabetes or insulin-dependent states.
  2. Pathophysiology: Insufficient insulin, leading to fat breakdown and ketone body production.
  3. Manifestations: Dehydration, nausea, deep rapid breathing, fruity scented breath.
  4. Diagnostics: Blood glucose levels, ketones in urine, arterial blood gases.
  5. Clinical Course: Acute complication, can be life-threatening without rapid treatment.
  6. Other: Emergency treatment with insulin and fluid replacement.
19
Q

HHNK-Hyperosmolar Hyperglycemic Nonketotic Syndrome

A
  1. Etiology: Common in Type 2 diabetes with some insulin activity preventing ketosis.
  2. Pathophysiology: Severe hyperglycemia leads to osmotic diuresis and dehydration.
  3. Manifestations: Severe dehydration, altered consciousness, high blood sugars.
  4. Diagnostics: High blood glucose, increased serum osmolality, absence of significant ketosis.
  5. Clinical Course: Acute; precipitated by infections or other illnesses.
  6. Other: Prevent with adequate hydration and monitoring glucose levels.
20
Q

Adrenal Gland Function including RAAS

A
  1. Etiology: Adrenal glands produce vital hormones including cortisol, aldosterone.
  2. Pathophysiology: Involves hormone synthesis, release influenced by ACTH, angiotensin II.
  3. Manifestations: Changes in electrolyte balance, blood pressure, metabolism.
  4. Diagnostics: Blood hormone levels, ACTH stimulation test.
  5. Clinical Course: Varies based on underlying condition (Addison’s, Cushing’s).
  6. Other: Regular monitoring and adjustment of hormone therapy.

Cortex: produces glucocorticoids, mineralcorticoids, and sex steroids
corticosterone: incr bl gluc, cause protein breakdown, antiinflamm properties, CORTISOL
Medulla: produces epin/norep; Chromaffin cells (pheochromocytes)

21
Q

Renin-angiotensin-aldosterone system

A

Stim variables: nitric oxide, cAMP, diuretics, Epinepherine, norep, early part of day, erect posture
Inhibiting variables: Adenosine, angiotesnin II, Adrenergic blockers, Aldosterone, Recumbant position, Later part of the day

Incr Aldosterone: from Hypo K,
lead to hypoNA, HyperK, ACTH levels

22
Q

SIADH versus DI

A
  1. Etiology: SIADH: excessive ADH. DI: insufficient ADH.
  2. Pathophysiology: SIADH: water retention. DI: water loss.
  3. Manifestations: SIADH: hyponatremia. DI: polyuria, polydipsia.
  4. Diagnostics: Serum sodium, urine osmolality, water deprivation test.
  5. Clinical Course: Both require careful fluid and electrolyte management.
  6. Other: Medications, fluid management, monitoring.
23
Q

Hypopituitarism versus Hyperpituitarism

A
  1. Etiology: Impaired or excessive pituitary hormone production.
  2. Pathophysiology: Affects multiple endocrine pathways due to pituitary hormones.
  3. Manifestations: Vary based on specific hormones involved.
  4. Diagnostics: Hormone levels, MRI for pituitary tumors.
  5. Clinical Course: Depends on extent, rapidity of onset, and efficacy of treatment.
  6. Other: Hormone replacement or surgical removal of tumor may be indicated.
24
Q

Hyperthyroidism

A
  1. Etiology: Most often Graves’ disease.
  2. Pathophysiology: Excessive thyroid hormone production.
  3. Manifestations: Weight loss, anxiety, tremors, heat intolerance.
  4. Diagnostics: TSH, T3, and T4 levels; thyroid scan.
  5. Clinical Course: Can lead to complications like thyrotoxic crisis.
  6. Other: Anti-thyroid medications, radioactive iodine, or surgery.
25
Q

Hypothyroidism

A
  1. Etiology: Hashimoto’s thyroiditis, iodine deficiency.
  2. Pathophysiology: Insufficient thyroid hormone production.
  3. Manifestations: Fatigue, weight gain, cold intolerance, bradycardia.
  4. Diagnostics: TSH and T4 levels.
  5. Clinical Course: Lifelong, generally managed with hormone replacement.
  6. Other: Regular monitoring of thyroid function tests.
26
Q

Hyperparathyroidism versus Hypoparathyroidism

A
  1. Etiology: Overactivity vs. underactivity or damage to parathyroid glands.
  2. Pathophysiology: Altered calcium and phosphorus metabolism.
  3. Manifestations: Bone pain, osteoporosis vs. muscle cramps, tetany.
  4. Diagnostics: Serum calcium, parathyroid hormone levels.
  5. Clinical Course: Varies, may require surgery or calcium supplements.
  6. Other: Dietary management, regular monitoring.
27
Q

Chronic Complications of Hyperglycemia

A
  1. Etiology: Prolonged elevated blood glucose levels.
  2. Pathophysiology: Vascular damage, neuropathy.
  3. Manifestations: Cardiovascular disease, kidney damage, vision loss.
  4. Diagnostics: Regular monitoring of A1c, kidney function, eye exams.
  5. Clinical Course: Gradual, progressive.
  6. Other: Importance of maintaining good glucose control to prevent complications.
28
Q

Cushing’s Syndrome

A
  1. Etiology: Excess cortisol, often due to pituitary adenoma.
  2. Pathophysiology: Hypercortisolism.
  3. Manifestations: Weight gain, striae, hypertension, mood changes.
  4. Diagnostics: 24-hour urinary free cortisol, dexamethasone suppression test.
  5. Clinical Course: Potentially severe complications if untreated.
  6. Other: Surgery, radiation, or medical therapies as treatment options.
29
Q

Addison’s Disease

A
  1. Etiology: Autoimmune destruction of adrenal cortex.
  2. Pathophysiology: Insufficiency of cortisol and aldosterone.
  3. Manifestations: Fatigue, hyperpigmentation, low blood pressure.
  4. Diagnostics: ACTH stimulation test, electrolytes.
  5. Clinical Course: Chronic, potentially life-threatening in crisis.
  6. Other: Lifelong hormone replacement therapy, stress dose management.
30
Q

anterior pituitary hormones ( adenohypophysis)

A

FLATPiG
FH (follicle stimulating)
LH (leutenizing hormone)
ACTH (adrenocorticotropic hormone)
TSH (thyroid stimulating hormone)
Prolactin
GH (Growth hormone)

31
Q

neurocrine

A

neuronal travel to target cell

32
Q

endocrine

A

through blood to target cell

33
Q

paracrine

A

through interstitial fluid to work on cells in local area

34
Q

autocrine

A

works on self

35
Q

steroid hormone derived from

A

cholesterol

36
Q

up-regulation

A

increased number of receptors on the target cell
leads to incr cell energy
net incr of basal metabolic rate

37
Q

CA++ and Phos-what kind of relationship do they have?

A

indirect/inverse

pathophys (14 decks)

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