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Pathophysiology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

The pancreas is a ___ gland.

A

endocrine and exocrine

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2
Q

What does Glucagon do?

A

increased blood glucose via glycogenesis

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3
Q

What does Amylin do?

A

inhibits glucagon secretion after meals

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4
Q

What does Insulin do?

A
  • promotes glucose uptake in cells
  • promotes glucose storage as glycogen
  • prevents breakdown of glycogen and fat
  • inhibits glycogenesis
  • increases protein synthesis
  • increase k+ to cells
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5
Q

Pathology of diabetes mellitus

A
  • destruction of beta cells in pancreas
  • little to no insulin production
  • decreased amylin
  • hyper glycemia
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6
Q

Etiology of Type One Diabetes

A
  • most common auto-immune response
  • genetic predisposition
  • environmental trigger
  • not gender related
  • 10% of diabetes
  • earlier onset
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7
Q

Manifestations of Type One Diabetes

A
  • polyuria
  • polydipsia (thirst)
  • glucose in urine
  • cells are starving
  • breakdown of fats for fuel
  • fatigue
  • polyphagia (hunger)
  • fruity breath
  • recurrent infections
  • vision changes
  • paresthesias
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8
Q

Type One Diagnosis

A
  • history/physical exam
  • HbAIC
  • lab tests
  • ketouria
  • glucosuria
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9
Q

What types of lab tests are used for Type One Diagnosis

A
  • increased plasma glucose
  • fasting
  • glucose tolerance
  • random check
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10
Q

Why is a HbAIC test useful?

A

tests back months prior showing history of hyperglycemia

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11
Q

What is the Treatment for Type One Diabetes?

A
  • insulin (basal and after meals)
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12
Q

What is the pathology of Type Two Diabetes?

A
  • progressive impairment of beta cell function
  • progressive insulin resistance
  • decreased ability of insulin to act on target tissue
  • increased insulin production (exhausting pancreas)
  • exhausted beta cells
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13
Q

Risk Factors of Type Two Diabetes

A
  • central obesity
  • increased blood pressure
  • increased triglycerides
  • decreased HDL cholesterol
  • insulin resistance
  • family history
  • age
  • indigenous, asian, african ancestry
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14
Q

Etiology of Type Two Diabetes

A
  • unknown

- probably genetic and environmental

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15
Q

Manifestations of Type Two Diabetes

A
  • polys may be present
  • fatigue
  • recurrent infections
  • vision changes
  • overweight
  • dyslipidemia
  • increase blood pressure
  • abdominal obesity
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16
Q

Diagnosis of Type Two Diabetes

A
  • history/physical exam
  • HbAIC
  • lab tests
  • ketouria
  • glucosuria
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17
Q

Treatment of Type Two Diabetes

A
  • diet
  • exercise
  • oral hypoglycemics
  • insulin
  • bariatric surgery
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18
Q

Acute Complications of Diabetes

A
  1. Hypoglycemia
  2. Diabetic Ketoacidosis (DKA)
  3. Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNK)
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19
Q

Hypoglycemia

A
  • low blood sugar
  • caused by decrease food and increase hypoglycemic agent or exercise
  • fast onset
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20
Q

Manifestations of Hypoglycemia

A
  • confusion
  • increased heart rate
  • cool and clammy
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21
Q

Diabetic Ketoacidosis (DKA)

A
  • high blood glucose
  • caused by lack of insulin to meet needs
  • usually in type one
  • slower onset
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22
Q

Pathology of DKA

A
  • hyperglycemia leading to glucose in urine leading to polyuria leading to polydispia, hypotension, and tachycardia
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23
Q

Manifestations fo DKA

A
  • rapid weight loss
  • seizures
  • marked fatigue
  • coma
  • seizures
  • Kussmal resps (to compensate for metabolic acidosis)
  • fruity or acetone breath
24
Q

Treatment for DKA

A
  • insulin

- IV fluid

25
Q

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNK)

A
  • caused by infection or hospitalization

- very slow progression (slowest of three acute)

26
Q

Pathology of HHNK

A
  • hypre glycemia leading to glucose in urine leading to polyuria, polydispia, incrased BP, increased HR
27
Q

Manifestations of HHNK

A
  • profound fluid loss
  • no ketosis
  • much sicker than other two acute complications
28
Q

Chronic Complications of Diabetes

A
  1. Macrovascular Disease
  2. Microvascular Disease
  3. Neuropathiesis
  4. Infection
29
Q

Pathology of Chronic Complications of Diabetes

A
  • schwann cells
  • ion pumps
  • glucose binds with proteins in blood vessel walls trapping LDL and triggering inflammation
  • increased water in lense of eye
  • decreased antioxidents
  • increased inflammation
30
Q

Macrovascular Disease

A
  • artherosclerosis
  • MI
  • Stroke
  • peripheral artery disease
  • arterial foot ulcers
  • gangrenous feet
31
Q

Microvascular Disease

A
  • Ischemia of eyes and kidneys
  • retinopathy (number one cause of blindness in canada)
  • glaucoma
  • cateracts
  • nephropathy
32
Q

Neuropathies

A
  • ischemia to nerves and demylination
  • paresthesias
  • impaired pain sensation
  • gastric atrophy
  • paralytic bladder
  • impotence
  • to bladder , penis, gut etc.
33
Q

Infection

A
  • impaired WBC function

- increased glucose environment

34
Q

The Posterior Pituitary Secretes..

A

oxytocin and ADH

35
Q

Syndrome of Inappropriate ADH Secretion

A
  • too much ADH
  • results in reabsorption of water
  • decreased urine output
  • decreased serum sodium
  • hypotonic
36
Q

Diabetes Insipidus

A
  • not enough ADH
  • results in excretion of water
  • increased urine output
  • increased serum sodium
  • hypertonic
37
Q

What does the thyroid secrete?

A
  • T4 (thyroxin)
  • T3 (triiodothyronine)
  • calcitonin
38
Q

What does the thyroid do?

A
  • secretes hormones that increase metabolic rate or decrease serum Ca
39
Q

Hypothyroid

A
  • decreased thyroid hormone levels
40
Q

What is Hypothyroidism caused by?

A
  • Hashimoto’s Thyroiditis (autoimmue destruction of thyroid by T-cells)
  • more common in females
41
Q

Manifestations of Hypothyroidism

A
  • everything slows down
  • cold
  • heart failure
  • constipation
  • weakness
  • fatigue
  • decreased heart rate
42
Q

How is Hypothyroidism diagnosed?

A
  • confirmation of symptoms

- TSH checks (blood test)

43
Q

What is the treatment for Hypothyroidism?

A
  • medications (synthetic TSH)
44
Q

Hypothyroidism in Kids

A
  • cretinism

- thyroid hormones needed for physical and intellectual development

45
Q

Hyperthyroid

A
  • increased levels of thyroid hormone
46
Q

What is hyperthyroidism caused by?

A
  • Grave’s disease (type two auto immune)
  • antibodies bind to TSH receptors (mimics TSH)
  • common in females
47
Q

Manifestations of Hyperthyroidism

A
  • increased heart rate
  • weight loss
  • increased blood pressure
  • everything speeds up
  • polyuria
  • diarrhea
48
Q

How is Hyperthyroidism Diagnosed?

A

blood test for TSH

49
Q

What is the Treatment for Hyperthyroidism?

A
  • radioactive iodine
  • thyroid removal
  • thyroid suppressing meds (short term)
50
Q

Complications of Thyroid Conditions

A
  • exopthalamus (hyper)- protruding eyes

- periorbital edema (hypo)- swelling around eyes

51
Q

What does the Adrenal Cortex secrete?

A
  • glucocorticoids, mineralcorticoids, gonadotropins
52
Q

What does the Adrenal Medulla secrete?

A
  • epinephrine, norepinephrine regulated by HPA
53
Q

Hypercortisolism

A
  • Cushing’s Syndrome
  • adrenal tumor
  • ectopic ACTH production
  • latrogentic (long-term glucocorticoid therapy)
54
Q

Manifestations of hypercortisolism

A
  • round face
  • abdominal obeisity
  • buffalo hump
  • amenorrhea
  • poor wound healing
  • insulin resistance
  • hypocalcemia
  • osteoperosis
  • muscle weakness
  • ulcers
  • hypertension
  • thin wrinkled skin
  • abdominal striae
  • purpura
55
Q

What is Primary Hypocortisolism

A
  • addison’s

- rare

56
Q

What is secondary Hypocortisolism?

A
  • sudden withdrawal of glucocorticoid therapy

- gland atrophy during treatment

Pathophysiology (14 decks)

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