Brainscape's Knowledge GenomeTM

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


See full index

BOD 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

receptors occur on a different type of target cell located near the cells secreting the signaling molecules

A

paracrine signaling
(i.e fibroblast growth factor family0

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

receptors occur on the nuclear envelope of the cells that synthesized or internalized the signaling molecules

A

intracrine signaling
(i.e steroid hormone)

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

signaling molecule in vesicle (hormone of chemical messenger)
receptors occur on a different type of target cell located distant from the cells secreting the signaling molecules

A

endocrine signaling
(ie. thyroid stimulating hormone)

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

receptors occur on the plasma membrane of the same type of cell that secretes the signaling molecules

A

autocrine signaling (interleukin-1 in monocytes)

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

disruption in hormone causes___________

A

dysregulation in the controlled substance
Insulin/glucagon- glucose
Parathyroid/calcitonin - calcium
Aldosterone - Potassium

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

What is produced by the neurohypophysis

A

-Antidiuretic hormone (ADH) : acts on kidney tubules
-Oxytocin: acts on uterus smooth muscles and mammary glands

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

What are the 2 hormones produced by the acidophils in the pars distalis

A

-Prolactin
-Growth hormone

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

What is the only hormone without a recognized negative feedback from its target organ

A

Prolactin

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

anabolic through indirect effects leading to hepatic production of insulin growth like factor and cellular proliferation
Increased protein synthesis, mobilization of FA, decreased utilization of glucose are combination of both direct and indirect effects

A

Growth hormone

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

What is an example of a major counterregulatory hormone to insulin

A

Growth hormone
Glucocorticoids

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

Growth hormone results in:

A

Increased protein synthesis, mobilization of FA, decreased utilization of glucose
cellular proliferation

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

Acidophil or Basophil?
Prolactin

A

Acidophil

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

Acidophil or Basophil?
Growth hormone

A

Acidophil

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

Acidophil or Basophil?
FSH

A

Basophil

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

Acidophil or Basophil?
LH

A

Basophil

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

Acidophil or Basophil?
ACTH

A

Basophil

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

Acidophil or Basophil?
TSH

A

Basophil

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

contain no secretoy contents. May respresent stem cells or degranulated cells
in the pars distalis

A

Chromophobes

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

What serves as a substrate for every hormone produced in adrenal glands

A

Cholesterol

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

What are the layers of the adrenal cortex

A

Outer to inner
1) Glomerulosa- aldosterone
2) fasciculata- cortisol
3) reticularis - androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is produced in the zona glomerulosa

A

aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is produced in the zona fasciculata

A

cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is produced in the zona reticularis

A

androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When is renin produced

A

when the macula densa sense sense that there is a decrease in blood flow/cardiac output/perfusion to the kidneys
that converts angiotensin I to Angiotensin II to cause vasoconstriction and tells cortex to produce aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What converts renin from the macula densa cells to angiotensin I

A

angiotensinogen from the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What converts angiotensin I to angiotensin II

A

Angiotensin converting enzyme (ACE) from the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What stimulates the release of vasopressin/ADH

A

1) Hyperosmolarity
2) Hypovolemia/ Hypotension

pituitary releases it to vasoconstrict (Increased arterial pressure) and increase renal fluid reabsorption (increase blood volume and arterial pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the effects of vasporession/ADH

A

pituitary releases it to vasoconstrict (Increased arterial pressure) and increase renal fluid reabsorption (increase blood volume and arterial pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How might you get diabetes insipidus

A

1) Defect in the hypothalamus or posterior pituitary leading to inadequate ADH

2) Defect in the kidneys, insensitive to ADH, adequate ADH (nephrogenic )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Aldosterone has its action at the

A

distal renal tubule
-promote retention of Na+ and wasting of K+
-forms osmotic gradient that allows water to be saved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aldosterone allows for the retention of ______ and the wasting of ______

A

retention of Na+ and wasting of K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the effects of glucocorticoids

A

1) Promotes hepatic gluconeogenesis
2) Inhibits glucose uptake and metabolism in peripheral tissues (insulin counter-regulatory)
3) Directly increases lipolysis and redistributes fat via circulation
4) Promotes protein catabolism, impairs extracellular matrix
5) Promotes diuresis- inhibits vasopressin, increases GFR
6) Prevents arachidonic acid metabolism by phospholipase A2
7) Suppresses lymphocyte and macrophage function via lipid mediators and changes in growth factors IL-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What effect does glucocorticoids have on lymphocytes and macrophages

A

suppresses them and changes IL-2 growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What effect does glucocorticoids have on vasopressin

A

It inhibits vasopressin
-promotes diuresis and increases GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How can you tell what the acidophils and basophils secrete in the pars distalis

A

need to do IHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what produces catecholamines such as epinephrine and norepinephrine

A

the medulla of the adrenal gland- chromaffin cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the thickest layer of the adrenal cortex

A

zona fasciculata (produces glucocorticoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the appropriate ratio of medulla to cortex in the adrenal gland

A

1:1 medulla to cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what color does the adrenal medulla stain

A

purple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is an example of primary hyperfunction

A

androgen-producing tumors of the adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is an example of primary hypofunction

A

immune-mediated destruction of the thyroid or adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is an example of secondary hyperfunction

A

hypercortisolism due to ACTH-productng tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is an example of secondary hypofunction

A

uncommon- target tissue dysfunction: insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What can cause endocrine hyperfunction

A

1) Functional neoplasia / Abnormal feedback (ex: tumor)
2) Exogenous hormone administration
3) Hormone like substances (PHrp)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What can cause endocrine hypofunction

A

1) Non-functional neoplasia (pituitary)
2) Inflammatory destruction (usually autoimmune)
3) Congenital defects
4) Defects in hormone production or release
5) Idiopathic atrophy
6) Failure of tropic hormone secretion
7) Insensitivity of target organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Since hormones often have multiple functions,_______________ are common

A

secondary lesions in distant organ systems are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the signalment of dogs with hyperadrenocortism

A

Older dogs
polyphagia and weight gain
PU/PD
Pustular “skin disease” +/- hard bone like plates
occasionally acute respiratory distress (thrombosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What CBC findings will you see in a dog with Cushings

A

Lymphopenia
Mild neutrophilia - Stress leukogram
Mild thrombocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What Chemistry findings will you see in a dog with cushings

A

-Modest hyperglycemia - 170 mg/dl
-Hypercholesterolemia
-Marked and disproportionate elevation in ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What UA findings will you see in a dog with Cushings

A

Specific gravity of 1.013

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is seen clinically with dogs with Cushings

A

Clinical: Older dogs, polyphagia and weight gain, PU/PD
Pustular “skin disease” +/- hard bone like plates,
occasionally acute respiratory distress (thrombosis), pendulous abdomen, hepatomegaly, muscle atrophy, alopecia (no growth)

CBC: Lymphopenia, Mild neutrophilia - Stressleukogram
Mild thrombocytosis

Chem: -Modest hyperglycemia - 170 mg/dl, Hypercholesterolemia, Marked and disproportionate elevation in ALP

UA: Specific gravity of 1.013

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What might you see on necropsy of a dog with pituitary Cushings

A

-Bilateral Adrenalocortical hyperplasia (pituitary)
-adenoma/carcinoma on pituitary
-Enlargement of the Adrenal Cortex (no longer 1:1 to the medulla)
-Acute/Chronic renal infarct (thrombi) - tissue dies from coagulative necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How do you find the adrenal glands

A

find the phrenicoabdominal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

T/F: Cushing dogs hypercoagulable

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How might an animal die from cushings disease acutely?

A

Hyercoagulability
-Deep vein thrombosis and pulmonary thromboembolism as a result of both increased coagulation factors and decreased anti-thrombin III
-Pulmonary thromboemoblism- high V/Q mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Why do we see glycogen being stored in the liver with cushings disease

A

cortisol promotes glucagon and inhibits insulin function

stores instead of being properly being used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What occurs during dermal mineralization in cushing dogs

A

collagen is broken down and replaced with mineral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

85% of dogs with hyperadrenocorticism are

A

pituitary caused
Adenoma in the pars distalis leading to excessive primary secretion of ACTH -> Cortisol is secreted with no sensitivity to negative feedback
Bilateral adrenal cortical hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What effects on the adrenal glands will you see with pituitary dependent HA

A

bilateral cortical hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

With adrenal dependent HA, there is

A

contralateral cortical atrophy
excessive cortisol production
Inhibition of ACTH secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What might be a non-neoplastic, age related pituitary form of Cushings

A

older dogs have increased monoamine-oxidase leading to increased degradation of dopamine in CNS leading to decreased negative feedback of pituitary corticotrophs

Persistent secretion of ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

The hypercoagulable state seen with hyperadrenocorticism causes:

A

1) Deep vein thrombosis
2) Pulmonary thromboembolism

*From increased coagulation factors and decrease anti-thrombin III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hypercoagulable state seen in hyperadrencorticism is a result of and increase in _________ and a decrease in _______

A

Increased coagulation factors
Decrease anti-thrombin III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Pulmonary thromboembolism from a hypercoagulable state of hyperadrenocortism results in a

A

High V/Q mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What enzyme is increased in non-neoplastic, age-related, pituitary dependent hyperadrenocorticism

A

Increased monoamine-oxidase

Increases dopamine degradation in CNS, decrease negative feedback on piuitary corticotrophs
persistent secretion of ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is a result of increased monoamine-oxidase

A

Increases dopamine degradation in CNS, decrease negative feedback on pituitary corticotrophs
persistent secretion of ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the signalment of dogs with hypoadrenocorticism

A

Younger dogs (age 2-5 years)

Clinical history of intermittent hemorrhagic diarrhea
Acute-onset bradycardia
Cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is seen clinically of dogs with hypoadrenocorticism

A

Signs: younger dogs (2-5yr), intermittent hemorrhagic diarrhea, acute-onset bradycardia, cardiac arrest

CBC: Normal lymphocyte and neutrophil counts, mild non-regenerative anemia

Chemistry: hypoglycemia, hyperkalemia, hyponatremia, hypoand hypochloridemia, Azotemia with minimally concentrated urine (Na:K ratio of <25:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What CBC findings are seen in dogs with hypoadrenocorticism

A

Normal lymphocyte and neutrophil counts, mild non-regenerative anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What chemistry findings are seen in dogs with hypoadrenocorticism

A

hypoglycemia
hyperkalemia
hyponatremia
hypochloridemia
Azotemia with minimally concentrated urine (Na:K ratio of <25:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What Na:K ratio is typically seen in dogs with hypoadrenocorticism

A

<25:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do the adrenal glands look like on necropsy of a dog with hypoadrenocorticism

A

Diffuse atrophy of the adrenal cortex

*Large medullary region comparatively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What cell type is in the adrenal glands of hypoadrencorticism

A

lymphocytic adenolitis - autoimmune process

*hard to tell from this because it will be destroyed by the time the dog presents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is lost with canine hypoadrenocorticism

A

Adren cortical atrophy- loss of aldosteroen and cortisol, possibly hyperplastic pars distalis from elevated ACTH production

Loss of Na+ and retention of K+

Glucocorticoid: hypoglycemia and skin pigmentation-spill over of excess ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Why might an animal with Hypoadrenocorticism have a non-regenerative anemia

A

cortisol promote erythropoiesis
anemia may be compounded by gastrointestinal hemorrhage from the loss of mucosal integrity

76
Q

Hypoadrenocorticism result in (Hypo/hyperglycemia)

A

Hypoglycemia

77
Q

What is the signalment of PPID

A

Older horse- age >20years

Persistent lameness with radiographic evidence of chronic laminitis
Mild muscular atrophy
Unkempt and long hair coat, inconsistent with season
Overly docile mentality- changes in neurotransmitters
Moderate hyperglycemia

78
Q

What are some clinical signs of PPID

A

-Chronic laminitis
-Hypertrichosis-overproducing hair
-Hyperhidrosis
-Pendulous abdomen
-Epaxial muscle wastage

79
Q

What is the reason for overly docile mentality in horses with PPID

A

pituitary compressing on the brain above leading to impaired function of the hypothalamus

beta-endorphin

80
Q

How do you diagnose laminitis in horses on necropsy

A

take a saggital section of the hoof . if the coffin bone does not parallel the hoof wall and you have bulging of the tissue

81
Q

T/F laminitis is an inflammation issue

A

F: it is more of an architectural issue, mechanical issue and separation from the basement membrane
diagnose with PAS stain

82
Q

How do you diagnose laminitis on histology

A

PAS stain to look for architecture and disconnect from basement membrane

83
Q

What provides negative inhibition of the melanocytes in the pars intermedia

A

Dopamine

84
Q

Lack of ______ leads to increased POMC peptides- ACTH, MSH, b-END, and CLIP being produced

A

dopaminergic inhibition

85
Q

Where does the increased ACTH of PPID come from and what causes it

A

Increased ACTH from the pars intermedia due to decreased dopamine inhibition of the pars intermedia

86
Q

Normally when doing a TRH test, shows that when you give TRH, __________ but abnormally when TRH is given __________

A

Normal: MSH increases
Abnormal: ACTH increases

87
Q

Some clinical signs of PPID can be attributed to hypothalamic derangement from pressure of enlarging pituitary, such as

A

-Muscle wasting and PU/PD manifested because of elevated glucocorticoids + nervosa compression with impaired ADH secretion

-Elevated b-endorphin causes altered mentality

88
Q

PPID-associated laminitis

A

50% of PPID have laminitis
2/3 of laminitis is associated with hyperinsulinemia
Hyperglycemia and peripheral insulin resistance at the root of laminitis
Pathogenesis is poorly understood
-Glucose deprivation to laminae that may be driven by ACTH
-Results in insulin resistance and hyperinsulinemia similar to type 2 diabetes mellitus
-Hyperphagia?
-Pain relief from endogenous b-endorphin

89
Q

What is the typical signalment for feline acromegaly

A

Typically older cats, age >10 years
mentally dull and non-responsive upon presentation

Severe hyperglycemia >250mg/dl
stress leukogram and mild erythrocytosis
Elevated liver enzymes
Hyperphosphatemia without renal azotemia, mild proteinuria present
UA shows marked glucosuria

90
Q

Is feline acromegaly congenital or acquired

A

acquired

91
Q

What age of cats are typically impacted by acromegaly

A

typically older cats, age>10 years

92
Q

What facial differences are seen with feline acromegaly

A

Broadened maxilla
Protruded mandible
Ears pushed back

*oppositional bone growth

93
Q

Growth hormone induces

A

IGF-1

94
Q

25% of cats with diabetes have

A

unbeknownst acromegaly

95
Q

What causes acromegaly

A

an acquire excess of growth hormone secretion due to acidophil adenoma of the pars distalis

96
Q

What changes in the pancreas will you see with acromegaly

A

*Swollen (degeneration) and vacuolated B cells overporducing insulin to counteract the insulin resistance
alpha and delta and epsilon cells are pushed in the middle

islet amyloidosis

97
Q

How do cats with acromegaly typically present

A

with renal failure - proliferative glomerular nephropathy

with uncontrolled diabetes (Type 2 diabetes mellitus due to growth hormone mediated resistance- down regulation of insulin receptors on the target cells)
Prolonged insulin secretion and beta cell exhaustion

98
Q

What is a congenital excess of growth hormone called

A

gigantism

99
Q

What is the pathogenesis of acromegaly

A

1) Excess production of growth hormone due to acidophil adenoma of pars distalis
2) Excess production of IGF-1 leading to appositional bone growth, visceral organomegaly, nodular proliferative changes in pancreas, kidney and glomerular disease with proteinuria
3) GH induced reabsorption of phosphate
4) True erythrocytosis due to IGF-1 effects on bone marrow
5) Lack of ketosis due to altered fat metabolism
6) Likely associated with cardiomyopathy

100
Q

What effects does IGF-1 have on the bone marrow

A

causes a true erythrocytosis

101
Q

How do you diagnose acromegaly

A

1) measure IGF-1 in blood
2) follow up with a CT

102
Q

What portion of the adrenal gland do tumors typically develop in ferrets

A

Zona reticularis- androgens producing

103
Q

What is the signalment for ferrets with androgen-producing tumors of the adrenal cortex

A

middle aged ferret 5-7 years

104
Q

What clinical signs do ferrets get if they have androgen-producing tumor of adrenal cortex

A

Alopecia (total body) and dermatopathy
Palpable+painful abdominal mass
Pale mucus membranes, petechiae
Females: vulvar swelling
Males: prostatic hyperplasia

Non-regenerative anemia, thrombocytopenia, leukopenia (from estrogen immunosuppression)

105
Q

What do male ferrets with androgen-producing tumor of adrenal cortex typically get

A

Prostatic hyperplasia

106
Q

What do female ferrets with androgen-producing tumor of adrenal cortex typically get

A

Vulvar swelling

107
Q

Are androgen-producing tumor of adrenal cortex in ferrets metastatic

A

Yes but dont really tend to

108
Q

What is the main detriment to ferrets with androgen-producing tumor of adrenal cortex

A

effects of estrogen on the bone marrow
should have around 50-75% hematopoietic cells for their age and they have around 20%

109
Q

What might be the cause of androgen-producing tumor of adrenal cortex in ferrets

A

-Photoperiod being altered
-Chronic stimulation of zona reticularis by LH results in proliferative lesions

110
Q

Why is pancytopenia seen as a result of bone marrow aplasia in ferrets with androgen-producing tumor of adrenal cortex

A

poorly understood
myelopoiesis-inhibitory factor

111
Q

androgen-producing tumor of adrenal cortex in the ferret is caused by what two things

A

1) Bilateral cortical hyperplasia (45%)
2) Neoplasia of the zona reticularis (55%): carcinoma > adenoma

112
Q

What can cause prostatic squamous metaplasia in male ferrets

A

High levels of secreted estrogen compounds from androgen-producing tumor of adrenal cortex

113
Q

Rupture of prostatic cysts can lead to

A

prostatis are keratin is being released

114
Q

What might result from an enlarge prostate due to androgen-producing tumor of adrenal cortex

A

Rupture of prostatic cyst leading to keratin release and suppurative prostatis

Dysuria from enlargement

115
Q

What is a tumor of the adrenal tumor

A

pheochromocytoma
-may or may not release catecholamines

116
Q

What is the signalment for pheochromocytoma

A

multiple species but most frequently older dogs and aged cattle

117
Q

What are the clinical signs of canine pheochromocytoma

A

acute onset blindness (hypertension- retinal detachment)
bilateral mydriasis
tachyarrythmias
dyspnea

unremarkable clinpath - mild hyperglycemia

118
Q

Are pheochromocytomas malignant?

A

Yes very much so, very high unlike other adrenal processes

119
Q

Where to pheochromocytomas typically spread to

A

invasion into the vena cava, obstruct blood flow, can cause infarction
tumor emboli

120
Q

T/F pheochromocytomas cause retinal deteachment

A

True: from hypertension

121
Q

What is implicated in the development of pheochromocytoma

A

calcium homeostasis
-hypercalcemia and excess vitamin D result in chromaffin cell proliferation

122
Q

What can result due to a pheochromocytoma?

A

-Catecholamine induce cardiomyopathy (beta adrenergic stim leading to vasoconstriction and coronary vasospasm leading to myocardial infarction
-Retinal detachment
-paroxysmal hypertension

123
Q

Thyroperoxidase

A

oxidizes iodide (I-) to iodine (I2) in the colloid

124
Q

Describe the process of generating T3 and T4

A

Iodide (I-) from the blood moves through the cell to the lumen and is oxidized to iodine (I2) in the colloid by thyroperoxidase

CHO modification on Tyr occurs to make thyroglobulin and is released into the colloid

Thyroglobulin binds I2 on Tyr to become iodinated thyroglobulin

Endocytosis of colloid -> digestion of iodinated thyroglobulin to generate T3 and T4 which diffuse out of the cell into adjacent capillaries

125
Q

What are the effects of thyroid hormone

A

-Increased metabolism of fats and carbs, protein synthesis
-Cardiovascular- increases HR, contractility, and CO
-Nervous System- enhance sympathetic nervous system and mental activity
-Nearly every cell in body some effect
-Developmental biology

126
Q

What are the mechanisms of thyroid destruction

A

1) Atrophy- lack of trophic stimulation (pituitary neoplasia/destruction)
2) Inflammatory- autoimmune thyroiditis
3) Neoplasia (Non functional thyroid tumors- usually carcinoma and nonthyroid neoplasia- lymphoma)

127
Q

Non-functional thyroid tumors leading to thyroid destruction is normally caused by

A

carcinoma

128
Q

What are the mechanisms of thyroid proliferation

A

1) functional neoplasia- usually adenoma
2) adenomatous hyperplasia

129
Q

functional neoplasias leading to proliferation of thyroid is usually cased by

A

adenoma

130
Q

What is the cause of canine hypothyroidism

A

Primary is most common
Destruction/loss of the follicles
a) idiopathic follicular atrophy
b) lymphocytic thyroiditis
c) non-functional tumor, amyloidosis
Defect of thyroid hormone production

131
Q

Is hypothyroidism in dog caused by atrophy of the thyroid gland?

A

not technically
not a concern with the thyroid stimulating hormone

pituitary is still functional and the destruction of the thyroid isnt producing T3/T4. TSH will be high

132
Q

What is the most likely cause of hypothyroidism in livestock

A

nutritional from iodine deficiency- defect of thyroid hormone production
-goiter

133
Q

What are the lesions seen with hypothyroidism

A

-obesity with normal to decreased eppetite
-Changes in mentation,activity level
-skin changes: alopecia, pigmentation, myxedema
-heat seeking behaviors

134
Q

Hypercholesterolemia seen in hypothyroidism leads to

A

artherosclerosis

135
Q

what is the only time you see artherosclerosis in domestic species

A

hypothyroidism

136
Q

where do you normally see artherosclerosis in hypothyroid dogs

A

coronary arteries on heart
cerebral arteries going to brain
hepatmegaly, lipidosis
Glomerular, Corneal lipidosis

137
Q

What is the pathogenesis of atherosclerosis

A

decreased thyroid hormone
Decreased lipid metabolism/utilization
Hypercholesterolemia
endothelial damage
increased permeability
mobilization of macrophages
atherosclerosis

*Thrombosis is a major concern

138
Q

What is seen in the skin lesions of hypothyroidism

A

-Symmetrical alopecia
-Hyperpigmentation
-Epidermal/Dermal atrophy
-Myxedema

139
Q

What is the pathogenesis of alopecia in hypothyroidism

A

Hypothyroidism
No stimulation of follicular epithelial cells
Increased number of follicles in telogen (resting state)
progressive alopecia

140
Q

What are the causes of secondary hypothyroidism

A

-atrophy: T3/T4 synthesis is intact but stimulation of TSH is lost (Destructive pituitary lesion)

-goiter: inadequate thyroxine synthesis (low T3/T4) - iodine deficient diets (lambs, pigs, foals), goitrogenic compounds, genetic defect in enzymes or thyroglobulin
hypothyroid but proliferative lesion

141
Q

You get an excessive colloid appearance
and atrophic thyroid cells

A

True thyroid atrophy
-Secondary Hypothyroidism
no TSH production

142
Q

What is the pathogenesis of goiter

A

Follicular cells cant make T3/T4 -> pituitary increase release of TSH -> thyroid hyperplasia/hypertrophy

143
Q

How might you get inadequate thyroxine synthesis (low T3/T4)

A

1) Iodine deficient diets (lambs, pigs, foals)
2) genetic defect in enzymes or thyroglobulin
3) goitrogenic compounds

144
Q

What cells make T3/T4

A

follicular cells

145
Q

How do goitrogenic compounds interfere with thyroxine synthesis

A

-Interfere with iodine transport by trapping it
-Iodine cant be added onto surface of the thyroglobulin molecule
-processing into active hormone

146
Q

What are the clinical signs seen in cats with hyperthyroidism

A

-Increased basal metabolism (Weight loss with increased appetite)
-Renal: PU/PD, Increased GFR
-Cardiovascular system: tachycardia, hypertension, cardiac hypertrophy, detached retina
-GI: vomiting, diarrhea/bulky stool

Increased liver enzymes (ALT, ALP, AST)
70% also have signs of hyperparathyroidism
+/- azotemia
High T3/T4

147
Q

How do cats end up with hyperthyroidism

A

Primary Hyperfunction

Functional proliferative lesion
-unilateral or bilateral
-nodular hyperplasia (multinodular adenomatous hyperplasia
-Adenoma
-Adenocarcinoma (uncommon)

148
Q

What is the most common cause of death in cats with hyperthyroidism

A

cardiac hypertrophy
-narrowing of lumen and increased heart wall width
-endocardial fibrosis- can lead to a a thrombus

149
Q

saddle thrombus

A

a thrombus lodged in the iliac artery- causes tissue necrosis to both of the back legs

150
Q

How does hyperthyroidism result in a saddle thrombus

A

hyperthyroid
cardiomyocyte hypertrophy
turbulent flow
LA/LV thrombosis
Thromboembolism
Saddle thrombus

151
Q

Do cats normally get thyroid adenomas or carcinomas

are they functional?

A

follicular adenoma - functional

152
Q

Do dogs normally get thyroid adenomas or carcinomas?

are they functional?

A

Follicular carcinoma
non functional
but aggressive

153
Q

Do bulls normally get thyroid adenomas or carcinomas

are they functional?

A

Parafollicular adenoma or carcinoma- functional

154
Q

Do horses normally get thyroid adenomas or carcinomas

are they functional?

A

follicular adenoma < parafollicular cell adenoma

155
Q

follicular cell carcinoma

A

more common than adenomas in dogs

fixed, locally invasive

unilateral> bilateral
high metastatic potential
lungs and distant organ > lymph nodes

156
Q

What cells make parathyroid hormone

A

chief cells of parathyroid

157
Q

PTH is secreted in response to

A

hypocalcemia (low ionized Ca2+)

158
Q

What do parafollicular cells make

A

calcitonin
(decreases calcium levels)

159
Q

What does parathyroid secretion result in

A

1) Osteoclasts- liberate Ca2+
2) Kidney reabsorption
3) active Vitamin D activation to function to increase absorption of Ca and P in the GI

160
Q

What are the target organs of PTH

A

1) Bone: Ca2+ and PO4 out of the bone into the blood

2) Kidney: increased Ca2+ absorption in distal convoluted tubule, decreased PO4 absorption in proximal tubule
Ca2+ increase in the blood, decrease in urine
PO4 decrease in bloodm increase in urine, increased VitD conversion

3) Increased absorption of vitD and both Ca2++ and PO4 -> increase both in blood

161
Q

Primary hyperPTH

A

proliferative
-hyperplasia (multifocal/nodular)
-functional neoplasms: parathyroid adenoma > carcinoma (unilateral)

162
Q

Is functional parathyroid adenoma or carcinoma more common

A

adenoma

163
Q

Secondary hyperPTH to target organ dysfunction

A

Hyperplasia (diffuse, bilateral)
-renal or nutritional secondary hyperPTH

164
Q

Pseudohyperparathyroidism

A

Hypersecretion of hormone analog PTHrP seen in lymphoma, anal sac apocrine gland adenocarcinoma, multiple myeloma
bilateral atrophy of parathyroid gland

165
Q

What conditions if PTHrP seen in

A

lymphoma, anal sac apocrine gland adenocarcinoma, multiple myeloma

166
Q

What do parathyroid adenomas look like

A

large mass encompassing the entire parathyroid gland
defined margin

167
Q

What effect does increased PTH have on intestine

A

increased intestinal Ca2+ and PO4 absorption

168
Q

What effect does increased PTH have on kidney

A

Decreased Ca2_ excretion
Increased PO4 excretion
Increased Vit D activation

169
Q

What effect does increased PTH have on bone

A

Increased bone resorption

170
Q

What effect does increased PTH have on blood

A

Increased Ca2+ : PO4 ratio

171
Q

How can you get secondary hyperparathyroidism

A

1) Nutritional - too little calcium, too much phospohrus, too little vitamin D

2) renal disease: impaired nephron function leading to P retention, loss of Ca -> hyperparathyroidism

172
Q

How do you get nutritional secondary hyperparathyroidism

A

Diet with either
too little calcium
too much phsophorus
Too little Vitamin D

173
Q

If an animal has secondary hyperparathyroidism from either nutritional deficiencies or kidney disease, how does this appear on necropsy

A

Hyperplastic parathyroid
-increased signaling from too little calcium, too much phosphorus or too little vitamin D

174
Q

How do you get secondary hyperparathyroidism from kidney disease

A

impaired nephron function leading to P retention, loss of Ca, decreased vit D, and metabolic acidosis

leads to increased ionized Ca2+, decreased intestinal Ca2+ and PO4 absorption, and increased Ca2+ and PO4 binding

-Decreased serum Ca2+
-IIncreased PTH and bone resportion

175
Q

If Ca * PO4 is 60-70 what begins occuring

A

tissue mineralization all over body-> destruction of function and tissue death

176
Q

Fibrous osteodystrophy

A

increased osteoclastic bone resorption
replacement with fibrous connective tissue
attempts at osteoblastic production of immature woven bone (poorly mineralized)

more common in reptiles

177
Q

increased osteoclastic bone resorption
replacement with fibrous connective tissue
attempts at osteoblastic production of immature woven bone (poorly mineralized)

A

Fibrous osteodystrophy

178
Q

Rickets

A

vitamin D deficiency

179
Q

hypoparathyroidism

A

primary: autoimmune parathyroiditis

Secondary: chemical/toxic injury- parathyroid gland removal

180
Q

C-peptide

A

surrogate of beta cell function

181
Q

For every ___ molecule of there is _____ C-peptide

A

1 insulin molecule to 1 C=peptide

182
Q

direct indicator of how much insulin an animal can make

A

C-peptide

183
Q

Is insulin anabolic or catabolic

A

anabolic -> energy used to build big molecules and store sugars and fat
-blood glucose levels decrease

184
Q

Is glucagon anabolic or catabolic

A

catabolic -> energy released from big molecules as they are broken down
-Blood glucose levels increase

185
Q

Is metformin beneficial

A

only when the cat has levels of detectable insulin. measure c-peptide

186
Q
A

BOD 3 (5 decks)

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