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Patho: pulmonary; cardi; hemo; GI; Urinary > Hormones > Flashcards

Hormones Flashcards

1
Q

Steroid vs non- steroid hormones (5- each)

A

Steroid:

  • lipid soluble
  • bound to a protein carrier
  • receptor on the INSIDE of target cell
  • mobil receptor model
  • rapid long lasting response

Non-steroid:

  • water soluble
  • unbound
  • receptor in the OUTSIDE of target cell
  • 2nd messenger model
  • short acting response
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2
Q

what is the Mobile-receptor model

A

Steroid hormone passes through the cell wall and binds to a receptor; that receptor complex then moves in to the nucleus; induces transcription; leading to translation= new protein made; that protein causes an effect.

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3
Q

what is the second messenger model

A

non-steroidal hormone CANNOT pass though the cell membrane; it binds to an external receptor; leading to the activation of an internal pathway change; activating second messenger

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4
Q

Which gland does the hypothalamus secret to?
Without the hormones the target glands will…
With excess hormone the glands will… EG…

A
  • anterior pituitary
  • not enough= atrophy
  • too much= undergo hyperplasia and hypertrophy

Hypertrophy and hyperplasia of the Thyroid gland: Hyperthyroidism

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5
Q

Anterior Pituitary

Posterior Pituitary

A

Adenohypophysis, “aneno”= gland, “A” think Anterior

Neurohypophysis, “neuro”, posterior

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6
Q

Adenohypophysis
Neurohypophysis
-the gland and the mode of communication

A
  • Hypothalamus communicates with the ANT PIT by secreting regulatory hormones into the BLOOD STREAM (via infundibula)
  • Hypothalamus communicates with the POST PIT by direct NEURONAL connections

After simulation they each release their hormones into systemic blood supply

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7
Q 
Thyroid Hormone (TH)
Function (4)
A

Affects growth and maturation of tissues, cell metabolism, heat production, and oxygen consumption

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8
Q

Calcitonin
who secretes it
function

A

Secreted by the thyroid

  • Regulation of blood calcium and bone density
  • Inhibition of osteoclasts/ stimulation of osteoblasts
  • Too much Ca++ in the blood= secrete calcitonin to move Ca++ into bone (increasing its density)
  • Calcitonin decreases blood Ca++ and increases bone density!
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9
Q

Parathyroid Hormone function
hypersecretion
hyposecretion

A

-Antagonist (works opposite) to Calcitonin
-Stimulation of osteoclasts (bone breakdown, increasing Ca++ in blood)
hypersecretion leads to osteoporosis
hyposecretion leads to decreased vit D release from kidney

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10
Q

Pancreatic Islet Cells (2)

function

A
  • Alpha cells – secrete Glucagon

- Beta cells – secrete Insulin

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11
Q

Alpha cells

Beta cells

A

-secrete Glucagon
“you secrete glucose when your glucagon is gone” (hypoglycemic)
Works in the liver to secrete glucose and raise blood sugar.

-secrete Insulin when hyperglycemic to lower blood sugar.
Works in the liver to take up glucose and store as glycogen.

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12
Q

How do beta cells work to facilitate the rate of glucose uptake by cells?

A

Glucose requires facilitated diffusion to enter cell. Insulin binds in insulin receptors and stimulates the opening of the glucose channel.
Therefore insulin is the KEY that allows our cells to take up sugar

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13
Q

How do alpha cells work to increase blood glucose?

A

The liver is stimulated:

  • Glycogenolysis- breakdown of glycogen
  • Gluconeogenesis- formation of glucose from non-sugar products
  • Lipolysis- break down of fat into sugar, keto body
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14
Q 
Adrenal cortex (3 hormones)
80% of an adrenal gland’s total weight

Adrenal medulla (1)

A
  • Aldosterone
  • Cortisol
  • Weak androgens and estrogens

Innervation by SNS
-Catecholamines (Epi/norepi) into blood

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15
Q

Adrenal Cortex

3 layers and what they regulate

A

1) Glomerulosa (salty)- Mineralcorticoids (aldosterone), regulates Na+
2) Fasciculata (sweet)- Glucocorticoids (cortisol), increase blood glucose
3) Reticularis (sex)- Weak Androgens (DHEA), sex development

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16
Q

(SALTY) Mineralocorticoids- Aldosterone
what it does
what this causes in the DCT
what it is regulated by

A

Aldosterone turns on Na+/K+ pump in the DCT and collecting duct of cells

↑ Na+ uptake
↑ Na retention with LOSS of K+ and H+

Regulation by the renin-angiotensin system

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17
Q

(SWEET) Glucocorticoids - Cortisol

A 
Released with bodily stress
↑ blood sugar by gluconeogenesis
Anti-inflammatory
Growth suppression
Influences awareness and sleep habits
Inhibits bone matrix-protein matrix (decrease bone density)
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18
Q

(SEX) Adrenal estrogens and androgens
estrogen and Androgens
function

A

Estrogen secretion is minimal (vs. ovary)
Needed in men b/c no ovary

Androgens – weak
DHEA
Converted by peripheral tissues to stronger androgens such as testosterone
Needed in women b/c no testes

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19
Q

Panhypopituitarism
what it is
cause

A

“pan”=all, “hypo”; ant pit hormones are low

Due to infundibulum damage

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20
Q

Hypopituitarism
what it is
cause
s/s

A

deficiency in 1 or more pituitary hormones

Usually due to pituitary infarction (narcotic effect of decreased blood flow)

21
Q

Hyperpituitarism
what it is
cause
s/s

A

hypersecretion of in 1 or more pituitary hormones

Commonly caused by a benign slow-growing pituitary adenoma
s/s:
Headache and fatigue
Visual changes (b/c a tumor is growing next to the optic tract, pushing on it)
Hyposecretion from those cells that are most sensitive to pressure from the growing tumor (FSH-and LH-secreting cells)

22
Q

Acromegaly

A

Hypersecretion of GH during adulthood
Increase metabolic effects (sim. to hypothyroidism)
Continued bone growth of nose, chin, hands, feet (will NOT grow in height)
Connective tissue changes (cardio and respiratory concerns)

23
Q

Hypersecretion of prolactin
what it is
cause
s/s: male vs female

A

(most common pit. adenoma)

Caused by prolactinoma

In a non-breast feeding females – amenorrhea, galactorrhea, hirsutism and osteopenia (loss of bone density)
In males – hypogonadism, erectile dysfunction, impaired libido, oligospermia and ↓ ejaculate volume

24
Q

SIADH
what it is
cause
s/s

A

Syndrome of inappropriate anti-diuretic hormone secretion (Hypersecretion of ADH)

Small cell lung cancer
Brain injury or infection (post op.)
Sepis
Psychiatric/drugs

Water intoxication (hyponatremia, hypoosmolality)
Decreased blood concentration, too much water in blood stream resulting in high BP and risk of ICP.
Low volume, high concentration urine output

25
Q

Polyuria

Polydipsia

A

Polyuria- excessive urine output

Polydipsia- excessive thirst

26
Q

what does Diabetes mean?

A

“to siphon” (water!)
Polyuria- excessive urine output
Polydipsia- excessive thirst
B/c water is being excessively siphoned out of the blood into urine

27
Q

Diabetes Insipidus vs Mellitus

A

Insipidus: Not sweet pee
ADH problem
No relationship to sugar

Mellitus: sweet pee
Excessive glucose in the urine (should have none)
Insulin problem 
Excessive hyperglycemia 
Type I and type II
28
Q 
Diabetes insipidus
what it is 
s/s
Neurogenic
Nephrogenic
Psychogenic
A

Insufficiency of ADH

Polyuria and polydipsia, hypernatremia, hypersomolality (thin concentration)
Inability to concentrate urine
Constantly dehydrated

-Neurogenic
Insufficient amounts of ADH
from post pit

-Nephrogenic
Inadequate response to ADH
from kidney

-Psychogenic (not really DI)
Excessive consumption leads to similar findings
(hypernatremia)

29
Q 
Hyperthyroidism
what it is
Main disorder 
s/s 
Thyrotoxic crisis
A

Increase T3 and T4- TRH and TSH are low due to negative feedback.
Graves- autoimmune: Antibodies binds to TSH receptor leading to inappropriate over activation of T4 and T3. The hypothalamus tries to turn down the over activation by turning down TSH.

Increased Metabolism: Warm/sweaty (fever), weight loss (hungry), thinning hair, tachy, insomnia, exopthalmos, goiter

Thyrotoxic crisis: prolonged thyrotoxicosis. Excessive stimulation the over works the heart, BP, leading to cardio events. Can be fatal.

30
Q

Thyrotoxicosis:

A

the state in which the entire body is experiencing the hyperthyroid effects
can result from dysfunction of the pituitary, the thyroid gland, ectopic thyroid tissue, or the ingestion of excessive amounts of TH medication

31
Q 
Hypothyroidism
what it is
Main disorder
s/s 
Myxedema coma
A

(most common thyroid disorder)
decreased T3 and T4; increased TRH and TSH to compensate
Hashimotos- autoimmune: antibody binds to T4 and T3 causing direct autoimmune attack to the thyroid.

Fatigue, weight gain (decreased hunger), hair loss, cold, brady, decrease HR, decrease BP (risk of coma)
Periorbital myxedema (bags around the eyes)
Goiter

Myxedema coma: low metabolic functioning leading to decreased neurologic function. Can be fatal

32
Q

Hyperparathyroidism
what it is
s/s

A

Excess secretion of PTH (antagonist to calcitonin) from one or more parathyroid gland.

Usually secondary to a chronic disease 
Hypercalcemia
Hypophosphatemia
Hypercalciuria: kidney stones
Pathologic fractures (from decreased bone density)
33
Q

Hypopararthyroidism

A

Abnormally low PTH levels leads to low blood Ca++ (thus leaning to hypocalcemic effects)

Usually caused by parathyroid damage during thyroid surgery

34
Q

Adrenal Cortex:
Cushing disease
Cushing syndrome

A 
Cushing disease (big cushion of steroids)
Excessive anterior pituitary secretion of ACTH (high cortisol levels)

Cushing syndrome
Excessive level of cortisol regardless of cause

35
Q

Diabetes Mellitus
what it is
s/s

A

Diabetes Mellitus = disorder of glucose metabolism related to insulin

Hyperglycemia- leading to the 3 P’s: polydipsia, polyuria, polyphagia. Weight loss, fatigue

36
Q

3 P’s of DM:

A
  • polydipsia: increased thirst from polyuria
  • polyuria: the PCT is maxed out and cannot absorb all glucose; it also attracts water!
  • polyphagia: tissues are not getting the resources they need; turns on hunger in the brain
37
Q

HbA1c (Glycated hemoglobin test)

A

Monitors long term (120 day) blood sugar levels to prevent severe cardiovascular and neurologic complications
Amount of sugar attached to hemoglobin during production in the bone marrow

38
Q

Type I
what it is
cause

A

(Insulin Dependent) =no insulin
Pancreatic atrophy and specific loss of beta cells and loss of insulin production

Typically early in life, BUT can be later in life

Due to genetic autoimmune (most common), viral attack on beta cells
Pancreatic damage: pancreatitis, trauma, resection

39
Q

Type II
what it is
cause

A 
(Insulin Resistant) =has insulin but it doesn't function
Prolonged hyperglycemia (years) leads to increased resistance by insulin receptors
Chronic type II, may lead to a loss of insulin (NOT type I, "insulin dependent")
More common (90%)
Risk factors: 
*Genetic susceptibility* 
Environmental factors- socioeconomic status (be kind).  
Obesity (diet and lifestyle)

Over time; decrease Beta cell response to plasma glucose

40
Q

Chronic Conditions of Diabetes Mellitus:

A

prolonged hyperglycemia destroying tissues leading to decreased vascular flow

41
Q

Microvascular disease (DM Types I and II)

A 
(small vessel)
Retinopathy
Nephropathy 
Neuropathy 
Infection (most concerning) decreased specificity, blood flow, immune functioning; especially peripheral leading to amputations
42
Q

Macrovascular disease (Type II)

A 
(large vessel)
Atherosclerosis!!! 
Coronary artery disease
Stroke
Peripheral artery disease
43
Q

Acute Conditions Primarily of DM Type I

A 
Hypoglycemia: Insulin shock or reaction
Diabetic ketoacidosis (DKA)
44
Q 
Acute Conditions Primarily of DM Type I:
Diabetic ketoacidosis (DKA)
A

Leads to serious complications
-decrease Insulin leading to increase counter regulatory hormones (Catecholamines, cortisol, glucagon, GH)

-Ketoacidosis from not having enough glucose and leads to the breakdown of fats & proteins

45
Q

Adrenal Cortex:
Addison disease
what it is
s/s

A

Hyposecretion of adrenocortical hormones
(decrease Aldosterone and cortisol)

Fatigue, orthostatic hypotension, syncope, hypoglycemia, hyponatremia, increase K

46
Q

Adrenal Cortex:
Conn disease
what it is
s/s

A

Hyperaldosteronism
Hypertension, myalgias, weakness, chronic headaches, increase Na, decrease K
(opposite of Addison)

47
Q

Adrenal Cortex:

Hypersecretion of adrenal androgens and estrogens

A

Feminization: happens to males

Virilization: happens to females

48
Q

Adrenal Medulla:
Catecholamine hypersecretion
can cause (2)
s/s

A

(NE, Epi)
Chromaffin cell tumor
Pheochromocytoma

Secretions on a continuous or episodic basis

Hypertension, headaches, sweating, tachycardia, tachypnea, anxiety, chest pain

Patho: pulmonary; cardi; hemo; GI; Urinary (10 decks)

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