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184 Cards in this Set
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- Back
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What are the three kinds of steroid hormones made by the adrenal cortex that are synthesized from cholesterol |
Mineralocorticoids Glucocorticoid Gonadocorticoids |
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What is a mineralocorticoid made by the adrenal cortex |
Aldosterone |
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What is a glucocorticoid made by the adrenal cortex |
Cortisol |
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What are gonadocorticoids made by the adrenal cortex |
Testosterone & Estrogens |
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What are the two parts of the adrenal glands and where are they |
Adrenal cortex - outside Adrenal medulla - inside |
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What does the adrenal medulla make |
Catecholamines |
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What are examples of catecholamines and what type of hormone are they |
Epi & NE Amino acid derivatives |
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What amino acid are catecholamines derived from |
Tyrosine |
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What are the three layers / zones of the adrenal cortex: include depth (How to remember them) |
Zona glomerulosa - outer Zona fasciculata - middle Zona reticularis - inner (GFR) |
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What does the zona glomerulosa produce (Way to remember it) |
Aldosterone (Salt) |
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What does the zona fasciculata produce (Way to remember it) |
Cortisol (Sugar) |
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What does the zona reticularis produce (Way to remember it) |
Testosterone and Estradiol (Sex) |
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How to remember what the zones of the adrenal cortex produce |
G - Salt F - Sugar R - sex The deeper you go the sweeter it gets |
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Cortisol What gland produces cortisol (and zone if applicable) What type of hormone is cortisol What is the stimulus for cortisol |
Gland: Adrenal cortex Zone: Zona fasciculata Hormone type: steroid Stimuli: ACTH & Stress |
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What is the general action of cortisol |
It is necessary to resist different types of physical and mental stress |
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What are the actions of physiologic levels of cortisol |
It increases fuel energy (especially glucose, but also increases amino & fatty acids) to sustain stress It is permissive for catecholamine effects (by potentiating Epi & NE - via cardiac contractility & vasoconstriction action of NE) |
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Why do heart attacks occur more frequently in the AM |
Cortisol levels are higher |
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What are the actions of pharmacological levels of cortisol |
It is anti-inflammatory, like in treating RA It is immunosuppressive, like for transplants |
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What are pharmacological levels of cortisol |
Abnormally high levels |
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Aldosterone What gland produces aldosterone (and zone if applicable) What type of hormone is aldosterone What is aldosterone’s target organ |
Gland: Adrenal cortex Zone: Zona glomerulosa Hormone type: Steroid Target organ: Kidney |
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What are stimuli for aldosterone (specify the main stimulus) |
Ang II — main Increased plasma K+ levels Decreased plasma Na+ levels Very high ACTH |
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Where does ACTH come from? What does the ACTH affect? |
It comes from the anterior pituitary It stimulates all of the adrenal cortex |
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What are the actions of aldosterone |
It increases Na+ reabsorption in the DT of the kidneys
By increasing the number of Na+/K+ ATPase pumps and passive Na+ channels Increased Na+ reabsorption increase H2O, which increases ECFV (BV) and BP |
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What is the name of adrenal insufficiency? What hormones are insufficient? |
Addison’s disease Cortisol & Aldosterone |
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What is Addison’s disease due to? |
Defect in adrenal cortex causing it to be unable to synthesize normal amounts of steroid hormones: cortisol and aldosterone |
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What is the level of ACTH in Addison’s Disease? Why? |
High because there is no negative feedback |
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What is the level of ACTH in Addison’s Disease? Why? |
High because there is no negative feedback |
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What are causes of Addison’s disease? Treatments? |
Cause: TB / long-term cortisol treatment / autoimmune Treatment: Synthetic cortisol & aldosterone |
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Symptoms of Addison’s Disease (indicate main ones) |
*Increased ACTH & CRH levels due to lack of negative feedback Decreased plasma glucose (hypoglycemia) Weakness Weight loss *Hyperpigmentation (bronzing) due to increased ACTH which increases melanin production *Hypotension *Hyponatremia (low plasma Na) & Hyperkalemia (high plasma K)
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What is hypersecretion of Cortisol called |
Cushing’s syndrome |
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What is hypersecretion of Cortisol called |
Cushing’s syndrome |
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Cause of Cushing’s syndrome |
May be due to excessive anterior pituitary secretion of ACTH, an adrenal tumor (cortisol is normally produced by the adrenal glands), or by an ACTH-secreting tumor in the lungs |
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Symptoms of Cushing’s syndrome (indicate main ones) |
*Hyperglycemia due to increase Pglucose *Weakness *Centripetal obesity (fat around middle) and buffalo hump (made of brown fat) Poor wound healing *HTN “Moon face” (and curly hair) |
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What is excessive Aldosterone secretion called |
Conn’s syndrome / Aldosteronism |
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What is the cause of Conn’s syndrome / Aldosteronism |
A functional tumor of the adrenal cortex |
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What are symptoms of Conn’s syndrome / Aldosteronism (indicate main ones) |
*HTN *Decreased plasma potassium (hypokalemia) (hypernatremia) Metabolic alkalosis |
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Androgens & Estrogens What gland are Androgens & Estrogens secreted from (and zone if applicable) What type of hormones are Androgens & Estrogens? What is the stimulus for Androgens & Estrogens? What are the target organs for Androgens & Estrogens? |
Gland: Adrenal cortex Zone: Zona reticularis Hormone type: Steroid Stimulus: ACTH Target organs: Gonads |
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General effects/actions of both androgens & estrogens |
Secondary sex characteristics Identical to those of gonadal origin |
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Effects/actions of Estrogens |
No physiological significance in women due to high estrogen production via ovaries before menopause |
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Effects/actions of testosterone |
Males: no significance due to high testosterone production via the testes Females: Libido & Source of estrogen in postmenopausal women as testosterone is converted to estradiol) |
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What occurs with excessive secretion of Androgens (T) |
Adrenogenital syndrome |
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What are symptoms of Adrenogenital syndrome |
Enlargement of penis / clitoris Premature puberty Masculinization (virilization) in females (i.e. bearded lady) |
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What occurs with excessive secretion of estrogen in males? What medication has this effect as well? |
Gynecomastia Risperdol |
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Gynecomastia symptoms |
Enlarged breasts Sometimes other secondary sex characteristics |
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What gland and region if applicable are Epi & NE secreted from? What type of hormones are Epi & NE? What is the stimulus for Epi & NE? What are the target organs for Epi & NE? |
Gland & region: Adrenal medulla Hormone type: Catecholamines (Amino acid derivatives) Stimulus: Increased SNS Target organs: Heart & Blood vessels |
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%age of Epi derived from Tyrosine? NE? DA (dopamine)? |
Epi: 80% NE: 20% DA: some |
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What is the action of Epi & NE? |
Increases SNS b/c they act on membrane alpha and beta receptors throughout the body to potentiate sympathetic drive |
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What are metabolic actions of Epi & NE? |
Increasing plasma glucose Inhibiting insulin secretion, which also increases plasma glucose |
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What disorder is caused by hypersecretion of Epi & NE? |
Pheochromocytoma |
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What is the cause of Pheochromocytoma |
A catecholamine secreting tumor of the adrenal chromoffin cells |
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Symptoms of Pheochromocytoma, including the main ones and what they are attributable to |
Most are directly attributable to the action of large amounts of circulating catecholamines *HTN *HA *Excessive swelling Hyperglycemia because of metabolic effects |
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What is unique about the pancreas |
It is both an exocrine and endocrine gland |
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What does the pancreas do as an exocrine gland |
It secretes digestive enzymes into the duodenum which is the first part of the SI |
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What are the endocrine secretory units of the pancreas |
Islets of Langerhans |
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What four cell types are there in the Islets of Langerhans in the pancreas What do these four cell types secrete |
Beta cells - Insulin Alpha cells - Glucagon D cells - somatostatin F / PP cells - pancreatic polypeptide |
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What is the hormone of energy storage? Of energy release? |
Hormone of energy storage: Insulin Hormone of energy release: Glucagon |
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What organ is glucose stored? What form is it stored in? |
Liver via glycogen |
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What does insulin do to plasma glucose? What does glucagon do to plasma glucose? |
Insulin: decreases plasma glucose by bringing it into cells and storing it in the liver via glycogen Glucagon: increases plasma glucose by catabolizing glycogen |
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Does insulin or glucagon dominate after a meal? During a fast? |
After a meal: insulin moves glucose into cells & stores it via glycogen During a fast: glucagon breaks down glycogen |
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Does insulin or glucagon dominate after a meal? During a fast? |
After a meal: insulin moves glucose into cells & stores it via glycogen During a fast: glucagon breaks down glycogen |
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What type of hormone is Insulin? What gland and cell type is Insulin secreted by? What are the target organs of Insulin? |
Hormone type: Protein Gland & cells: Beta cells of Islets of Langerhans of pancreas Target organs: Liver, Muscle, & Adipose |
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What is insulin’s stimulus? |
Increased plasma levels of glucose (as well as amino and fatty acids) stimulates beta cells to increase insulin |
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What is the overall action of insulin? |
Insulin leads to decreased plasma glucose levels (as well as fatty & amino acids) by converting to storage form |
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Actions of insulin on glucose |
Increasing membrane transport of glucose into most cells, especially skeletal muscle, liver, and fat cells, stimulating an enzyme that puts it into glycogen, its storage form |
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What metabolisms does insulin effect, putting into storage forms: name their storage forms |
Carbohydrate metabolism - increasing storage of glucose as glycogen Lipid metabolism - promotes storage of fatty acids as triglycerides Protein metabolism - anabolically taking up amino acids to form proteins via protein synthesis |
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What is an A1c level? What does it measure? |
It is a blood test that averages blood glucose for the past 2-3months It measures what percentage of hemoglobin is coated with sugar (aka: glycated Hgb) |
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What is DM I |
Lack of insulin via inadequate secretion of insulin |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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What is polyuria due to in DM I? |
Not due to ADH but due to osmotic pull of H2O without glucose |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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What is polyuria due to in DM I? |
Not due to ADH but due to osmotic pull of H2O without glucose |
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Why does ketonemia & ketonuria occur in DM I? What does this lead to? Is this found in DM II? |
Since there isn’t glucose the body uses fat for metabolism, causing hepatic production of ketone bodies due to high levels of free fatty acids This can lead to ketoacidosis which can possibly cause acetone breath This is not usually found in DM II |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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What is polyuria due to in DM I? |
Not due to ADH but due to osmotic pull of H2O without glucose |
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Why does ketonemia & ketonuria occur in DM I? What does this lead to? Is this found in DM II? |
Since there isn’t glucose the body uses fat for metabolism, causing hepatic production of ketone bodies due to high levels of free fatty acids This can lead to ketoacidosis which can possibly cause acetone breath This is not usually found in DM II |
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Why do chronic complications such as Renal, Blindness, & Amputations occur with DM I? Where do amputations usually occur? |
Due to effect on microcirculation Amputations frequently of the feet |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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What is polyuria due to in DM I? |
Not due to ADH but due to osmotic pull of H2O without glucose |
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Why does ketonemia & ketonuria occur in DM I? What does this lead to? Is this found in DM II? |
Since there isn’t glucose the body uses fat for metabolism, causing hepatic production of ketone bodies due to high levels of free fatty acids This can lead to ketoacidosis which can possibly cause acetone breath This is not usually found in DM II |
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Why do chronic complications such as Renal, Blindness, & Amputations occur with DM I? Where do amputations usually occur? |
Due to effect on microcirculation Amputations frequently of the feet |
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What does dehydration lead to |
Increased Hct due to less volume |
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Is DM I insulin dependent? DM II? |
DM I: insulin dependent DM II: non-insulin dependent |
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What is DM I caused by? What was it previously called and why? |
Cause: an autoimmune response against receptors on Beta cells that cause Beta cells to secrete inadequate insulin Previously called: juvenile onset diabetes because it usually occurs in young people, <15YO |
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What does DM I require? |
Exogenous insulin via shots, infusion, etc. |
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What are symptoms of DMI? Indicate the main ones |
*Hyperglycemia (which leads to ...) *Glucosuria (which leads to ...) *Polyuria Ketonemia (ketones in blood) & Ketonuria Chronic complications (Renal, blindness, amputation) Polydipsia (thirst) Polyphagia (hunger) *Dehydration (which leads to increased Hct) Decreased weight |
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What is polyuria due to in DM I? |
Not due to ADH but due to osmotic pull of H2O without glucose |
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Why does ketonemia & ketonuria occur in DM I? What does this lead to? Is this found in DM II? |
Since there isn’t glucose the body uses fat for metabolism, causing hepatic production of ketone bodies due to high levels of free fatty acids This can lead to ketoacidosis which can possibly cause acetone breath This is not usually found in DM II |
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Why do chronic complications such as Renal, Blindness, & Amputations occur with DM I? Where do amputations usually occur? |
Due to effect on microcirculation Amputations frequently of the feet |
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What does dehydration lead to |
Increased Hct due to less volume |
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Why does DM I lead to decreased weight? |
Because the body is metabolizing fat & protein due to lack of glucose |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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What can DM II be treated with, alone? How many cases of DM does DM II comprise? |
May be treated with diet / exercise alone Makes up about 90% of DM |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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What can DM II be treated with, alone? How many cases of DM does DM II comprise? |
May be treated with diet / exercise alone Makes up about 90% of DM |
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What was DM II previously believed to be caused by? |
By down regulation of insulin receptors, with increased insulin leading to decreased number of receptors |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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What can DM II be treated with, alone? How many cases of DM does DM II comprise? |
May be treated with diet / exercise alone Makes up about 90% of DM |
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What was DM II previously believed to be caused by? |
By down regulation of insulin receptors, with increased insulin leading to decreased number of receptors |
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What is the role of obesity in DM II? |
Adipose cells overproduce Tumor Necrosis Factor alpha (TNF a) and Resistin which both may alter insulin binding |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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What can DM II be treated with, alone? How many cases of DM does DM II comprise? |
May be treated with diet / exercise alone Makes up about 90% of DM |
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What was DM II previously believed to be caused by? |
By down regulation of insulin receptors, with increased insulin leading to decreased number of receptors |
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What is the role of obesity in DM II? |
Adipose cells overproduce Tumor Necrosis Factor alpha (TNF a) and Resistin which both may alter insulin binding |
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What is insulin excess called? What does this cause? |
Called: Hypoglycemia / Hyperinsulinism This causes too much glucose entering the cells |
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Symptoms of diabetic coma and their respective treatments |
Acidosis (ketoacidosis) - Bicarbonate Dehydration - Saline Increased plasma glucose - Insulin |
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What is DM II due to? |
Insulin resistance via receptor insensitivity due to a decrease in a protein necessary for glucose to pass through the insulin primed receptor into the cell |
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In what age is DM II most common? What was it formerly called? What is important in having DM II? |
Common among obese adults ; it used to be called Adult onset diabetes as it usually occurs in >40YO, but it now also occurs in children Hereditary is very important in DM II |
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What can DM II be treated with, alone? How many cases of DM does DM II comprise? |
May be treated with diet / exercise alone Makes up about 90% of DM |
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What was DM II previously believed to be caused by? |
By down regulation of insulin receptors, with increased insulin leading to decreased number of receptors |
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What is the role of obesity in DM II? |
Adipose cells overproduce Tumor Necrosis Factor alpha (TNF a) and Resistin which both may alter insulin binding |
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What is insulin excess called? What does this cause? |
Called: Hypoglycemia / Hyperinsulinism This causes too much glucose entering the cells |
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What are symptoms of Insulin excess / Hypoglycemia / Hyperinsulinism? What are these symptoms caused by?: both usually and rarely |
CNS symptoms: Convulsions, Coma, and Depression of respiratory centers leading to death Usually caused by insulin OD and rarely caused by tumor of islet cells |
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In short, what effect does glucagon have? |
The opposite of insulin |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
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What is the general action of glucagon? |
Increase levels of glucose, fatty acids, and amino acids by breaking down their respective storage forms: glycogen, triglycerides, and proteins |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
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What is the general action of glucagon? |
Increase levels of glucose, fatty acids, and amino acids by breaking down their respective storage forms: glycogen, triglycerides, and proteins |
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How does Glucagon affect the three types of metabolism? |
Carbohydrate metabolism: causes Hyperglycemia by increasing blood glucose levels via glycogenolysis Lipid metabolism: increases lipolysis (breakdown of triglycerides) Protein metabolism: decreases protein synthesis and increases catabolism of proteins into amino acids |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
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What is the general action of glucagon? |
Increase levels of glucose, fatty acids, and amino acids by breaking down their respective storage forms: glycogen, triglycerides, and proteins |
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How does Glucagon affect the three types of metabolism? |
Carbohydrate metabolism: causes Hyperglycemia by increasing blood glucose levels via glycogenolysis Lipid metabolism: increases lipolysis (breakdown of triglycerides) Protein metabolism: decreases protein synthesis and increases catabolism of proteins into amino acids |
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Does insulin or glucagon produce a hypoglycemic response? A catabolic response? |
Hypoglycemic: Insulin Catabolic: Glucagon |
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In short, what effect does glucagon have? |
The opposite of insulin |
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What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
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What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
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What is the general action of glucagon? |
Increase levels of glucose, fatty acids, and amino acids by breaking down their respective storage forms: glycogen, triglycerides, and proteins |
|
|
How does Glucagon affect the three types of metabolism? |
Carbohydrate metabolism: causes Hyperglycemia by increasing blood glucose levels via glycogenolysis Lipid metabolism: increases lipolysis (breakdown of triglycerides) Protein metabolism: decreases protein synthesis and increases catabolism of proteins into amino acids |
|
|
Does insulin or glucagon produce a hypoglycemic response? A catabolic response? |
Hypoglycemic: Insulin Catabolic: Glucagon |
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|
After a large meal, what would the plasma levels of glucose, insulin, and glucagon levels be? |
Glucose: High Insulin: High Glucagon: Low |
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|
In short, what effect does glucagon have? |
The opposite of insulin |
|
|
What type of hormone is Glucagon? What gland and cell is Glucagon secreted from? |
Hormone type: polypeptide Gland & cell: Alpha cells of the Islets of Langerhans in the pancreas |
|
|
What are the stimuli for Glucagon? |
Decreased levels of plasma glucose, amino acids, & fatty acids which leads to stimulation of alpha cells which release Glucagon which increases Pglu, Paa, & Pfa |
|
|
What is the general action of glucagon? |
Increase levels of glucose, fatty acids, and amino acids by breaking down their respective storage forms: glycogen, triglycerides, and proteins |
|
|
How does Glucagon affect the three types of metabolism? |
Carbohydrate metabolism: causes Hyperglycemia by increasing blood glucose levels via glycogenolysis Lipid metabolism: increases lipolysis (breakdown of triglycerides) Protein metabolism: decreases protein synthesis and increases catabolism of proteins into amino acids |
|
|
Does insulin or glucagon produce a hypoglycemic response? A catabolic response? |
Hypoglycemic: Insulin Catabolic: Glucagon |
|
|
After a large meal, what would the plasma levels of glucose, insulin, and glucagon levels be? |
Glucose: High Insulin: High Glucagon: Low |
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What is the most important regulator of insulin secretion? |
Plasma glucose levels |
