Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Review 2020 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

How is glucose made available to the body

A

Glycogenolysis: Glycogen breakdown— short term 6-12 hrs
Gluconeogensis: Production of glucose— Prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is insulin released from

A

Beta cells in the pancreas when glucose is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the counter regulatory methods for decreased glucose

A

glucagon, catecholamines, cortisol and growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is glucagon made and how does it work

A

alpha cells of pancrease.

Stimulates glycogenolysis via cAMP, phosphorylation of glycogen phosphorylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do catecholamines increase glucose

A

realsed via SNS stimulation from adrenal medulla

potienated glucagon’s activity of phosphorylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does gluconeogesis occur

A

pyruvate, lacatic acid, glycerol, and amino acids to form glucose
Cortisol mobilized protien and adipocytes for ammino acids and FFA; inhibits insulin and potientiates effects of glucagon/epi on the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is the brain glucose levels compared to the rest of the body

A

Dependent on plasma glucose (don’t make own) 30 % less in brain cells than blood.
GLUT-1 glucose transporter for the brain
Neuronal damage, decreased cerebral ATP, cellular swelling, oxidative damage
Sympathoadrenal response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the broad categories of hypoglycemia

A

Excess secretion of insulin/ insulin like factors
Decrease glucose production
Excess glucose consumption (includes drugs)
Suprious (polycythemia, leukocytosis, error-handling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is an insulinoma and common signs

A

Functional beta cell tumor
Signs are seen after meals and exercise
Middle to large breed dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are indicators on blood work of insulinoma

A

Hypokalemia due to insulin induced shift
low fructosamine levels
>30 insulin:glucose ratio supportive (can be seen with sepsis, non pancreatic neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the goal of medical management in insulinoma

A

Give enough dextrose for insulin there but no so much to increase insulin release.
glucacorticioids, glucagon CRI (short term)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does stress hyperglycemia occur

A

200-400 mg/dl
Catecholamine excess
Increase lactate is also associated with increase hepatic glucose production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does hyperglycemia with TBI occur

A

associated with catecholamine response
Degree of injury with degree of increase glucose
Generally don’t need insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which ketones will react with the urine dipstick

A

acetone and acetoacetate

Beta-hydroxybuterate will not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the renal thresholds for glucose in a cat and dog

A

Dog 180 mg/dl

Cat 300 mg/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does ketones mean with Diabetes mellitus

A

absolute or relative insulin deficiency promoting lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does hyperglycemic hyperosmolar syndrome occur

A

sustained an insult leading to a marked reduction of GFR.

Ability to excrete glucose impaired leads to abnormal retention in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are laboratory findings of hyperosmolar hyperglycemic syndrome

A

Glu > 600 mg/dl
Osm/Kg > 350
Does not usually have ketones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two types of diabetes

A

Type 1- insulin deficiency dogs; immune mediated destruction
Type 2- Insulin resistance Cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does insulin resistance occur

A

Through counter regulatory hormones (cortisol, epi, GH, progesterone elevated)
Exerts negative infulence on insulin sensitivity at the level of the insulin receptor or insulin signaling cascade

21
Q

What are the negative effects of hyperglycemia

A

Reactive oxygen species
Pro-inflammatory cytokines (TNF alpha, IL-6, IL1 beta) - insulin resitant state
impair leukocyte function
limits neovascularization and collagen synthesis

22
Q

How are ketones formed

A

increase glucose stimulates hormone sensitive lipase and FFAs released from adipocytes
FFAs metabolized to triglycerides, CO2/H20 or ketone bodies
Counter regulatory hormones released due to stress stimulate lipolysis leads to more FFAs

23
Q

What are the mechanisms for decreased potassium in DKA/HHS

A

Osmotic diuresis- lytes lost along to maintain electroneutrality
Insulin defiency decrease amount of K co transported into the cell
Acidemia K shifts out of the cells in exchange for H+
Hyperosmolality
Hypervolemia induced and increased aldosterone – increase renal los
Decrease GI uptake

24
Q

Why does potassium decrease when insulin is given

A

K+ will move into cell along with glucose (cotransport)

Acidemia improves K+ will shift into cells

25
Q

What are the overarching treatment goals of DKA

A

Restore effective circulating volume
rehydration and maintenance fluids
supplement lytes to correct or prevent defficiencies
Initiate insulin therapy to reduce glucose levels and ketone production
Identify and treatment underlying disease

26
Q

When would you consider bicarbonate treatment treatment in DKA

A

pH > 7.1 HCO3- < 8 mmol/L, with refractory hypotension, arrythmias, insulin resistance, stupor/coma despite adequate volume and lyte

27
Q

What are the negative effects of bicarbonate treatment in DKA

A

Worsen Decrease K, Ca and hyper Osom
Induce paradoxical CNS acidosis
Poorer outcome when administered

28
Q

What is the overarching treatment goal of HHS and when is insulin started

A

insulin should be started when patient adequately hydrated and fluids alone are decreasing gluc by < 50 mg/dl/hr
Insulin is generally dosed at 50% of DKA

29
Q

What are the areas of the adrenal gland

A

GFR; Glomerulosa, fasiculata, reticularis

Salt, Steroid, Sex

30
Q

What is pheochromocytoma

A

CAtecholamine producting tumors (medulla)
Intermittent supraphysiologic catecholemeins
Signs increase in sympathetic tone

31
Q

What improves mortality with surgery of pheochromocytoma

A

Phenoxybenzamine: alpha adrenergic antagonist

3 weeks prior to sx

32
Q

What is hyperaldosterism

A

Cats> dogs

autonamous secretion of aldosterone (adrenal cortical tumors, or hyperplasia)

33
Q

What signs do you see with hyperaldosterism

A

Nephron retains both Na and H20 which increases blood volume and leads to BP
HypoK due to potassium wasting properties

34
Q

What is the difference between primary and secondary hypoadrenocorticism

A

Primary- all three adrenal cortex regions affected with > 90% damage
Secondary: abnormal pituitary gland lack of ACTH or hypothalmus lack of CRH

35
Q

What are the effects of glucocorticoid deficency

A

decreased intravascular volume, decreased blood pressure, hypogylcemia, GI ileus
Increase ADH, leads to more H2O reabsorption as cortisol inhibits ADH release

36
Q

What does not interfere with ATCH stim test

A

Dexamethasone

37
Q

What is a corisol result of < 2 mcg/dl indicate

A

only 1% of dogs with addisons will have > 2

but 21% of dogs with < 2 mcg/dl have another disease due to ACTH stim

38
Q

How do you differentiate primary and secondary addison’s with plasma ACTH

A

Primary will have increased because no cortisol for negative feedback
Secondary will have less because will not be secreted

39
Q

What hormone level of Thyroid is consitent with thyroid storm

A

There isn’t a level

40
Q

Define myxedema

A

Protracted untreated Hypo T4 leads to hyaluronic acid accumulation within the dermis
extracellular fluid accumulates and skin thickening

41
Q

What is the MOA of ADH on the kidney

A

V2 receptor activated G-protien coupled adenycylase which is stimulated to increase cAMP leads to protein kinase A activation and results in insertion of aquaporin 2 water channel in the collecting duct tubular membrane

42
Q

JVIM 2019 When adjusted for age was DM associated with CKD in cats

A

yes

43
Q

JVIM 2019 What was the recommended starting dose for DOCP

A

1.5 mg/kg

Dogs < 3 yrs needed higher doses

44
Q

JVIM 2019 What has been shown with high doses of ketaconazole

A

Hypoadrenocorticism

Resoloves once discontinued

45
Q

What is the MOA of metforman

A

Does not affect beta cell production in pancrease
Requires body have insulin
* Enhances muscle sensitivity to insulin and increases glucose metabolism
Decrease hepatic gluconeogensis and glycogenolysis

46
Q

Why are dogs and Cats not able to get D3 from skin

A

Due to high activity of 7-dehydrocholesterol delta 7 reductase

47
Q

2017 AJVR How effective was cortisol induced ALP at diagnosis HypoAC

A

Not good

in combo with other lab good

48
Q

2017 Vet journal what was noted about cardiac function in cats with DM

A

Have diastolic dysfunction that progresses over a 6 month period

Board Review 2020 (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions