Brainscape's Knowledge GenomeTM

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


See full index

VTS(ECC) Preparation > Endocrine system & endocrine emergencies > Flashcards

Endocrine system & endocrine emergencies Flashcards

1
Q

This insulin type is immediate acting with a short duration, making it ideal for constant rate infusions, and can also be administered IV.
a. Porcine zinc insulin suspension (Vetsulin®)
b. Regular insulin
c. NPH insulin
d. Glargine insulin

A

B

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

Somogyi phenomenom, episodes of hypoglycemia followed by rebound hyperglycemia, should be treated by:
a. increasing the patient’s insulin dose
b. administering insulin TID instead of BID
c. decreasing the patient’s insulin dose
d. administering insulin SID instead of BID

A

C

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

Which of the following is a typical abnormality seen with hypoadrenocorticism crisis?
a. Hyperglycemia
b. Hypernatremia
c. Hyperkalemia
d. Azotemia

A

C

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

The signs and symptoms of typical hypoadrenocorticism are caused by inadequate secretion of:
a. glucocorticoids
b. mineral corticoids
c. both glucocorticoids and mineral corticoids
d. anabolic steroids

A

C

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

What test is used to confirm a hypoadrenocorticism diagnosis?
a. Basal serum cortisol
b. Fructosamine level
c. Adrenocorticotropic hormone test
d. Metanephrine level

A

C

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

In hyperosmolar hyperglycemic states, sodium concentrations should be reduced at what rate?
a. >0.5^mEq/L/h
b. <0.5^mEq/L/h
c. >0.2^mEq/L/h
d. <0.2^mEq/L/h

A

B

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

Inadequate control of diabetes mellitus would be indicated by a fructosamine level of which value?
a. 225^μmol/L
b. 280^μmol/L
c. 360^μmol/L
d. 540^μmol/L

A

D

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

Which of the following is not a ketone?
a. Acetyl CoA
b. Beta-hydroxybutyrate
c. Acetoacetate
d. Acetone

A

A

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

The formula [2 × (Na + K)] + (BUN/2.8) + (glucose/18) calculates what value?
a. Base excess
b. Base deficit
c. Serum osmolarity
d. Anion gap

A

C

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

A serum sodium to potassium ratio (Na:K) of <27 is indicative of which disease process?
a. Hyperadrenocorticism
b. Hypoadrenocorticism
c. Diabetic ketoacidosis
d. Hyperosmolar hyperglycemia syndrome

A

B

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

What makes up the endocrine system?

A

Adrenal glands
Parathyroid
Thyroid
CNS
GIT
Pancreas
Kidneys
Gonads
Placenta

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

Neurotransmitters….

A

Act locally to control nerve function and are released by axon terminals of neurons into the synaptic cleft

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

Endocrine hormones….

A

released by “glands” into circulating blood and influence the function of the target cells

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

Neuroendocrine hormones….

A

secreted by neurons and influence the function of their target locations

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

Paracrine substances….

A

Secreted by cells into the ECF and affect the function of neighbouring target cells of a different type

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

Autocrine substances….

A

Secreted by cells into ECF and affect the same cells which produce them

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

Cytokines….

A

proteins secreted by cells into the ECF that affect the immune system and can function as paracrine, autocrine or endocrine hormones

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

Three broad classes of hormones

A
  1. Proteins & polypeptides i.e. insulin & glucagon
  2. Steroids i.e. cortisol, aldosterone & testosterone
  3. Tyrosine amino acid derivatives i.e. thyroxine, epinephrine, norepinephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are all endocrine secretions controlled?

A

Tightly controlled through feedback mechanisms

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

Hormone receptor location

A

Large proteins that life on the surface or in the surface of cell membranes, cytoplasm or nucleus

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

What or how much a hormone exerts depends on

A
  • Rate of production or secretion
  • Availability if transport plasma proteins
  • Ability of target tissue to convert the hormone
  • Availability of the specific receptor
  • Breakdown of the hormone
  • Liver/Kidney ability to excrete
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hypothalmic-pituitary axis (HPA axis)

A

Hypothalamus co-ordinates the endocrine system. It releases corticotropin releasing hormone (CTRH) & other major hormones which is received by the pituitary gland causing the release of ACTH, GH, prolactin, LG, FSH. ADH is secreted from the posterior gland. The adrenal glands are signalled to release cortisol

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

Diabetes mellitus pathophysiology

A

Type 1 is insulin -dependent (congenital, immune-mediated, idiopathic) whereas type 2 is destruction of pancreatic b-cells (obesity, genetics, islet amyloidosis, abnormal insulin response). Approx. 50-70% of DM cases are type 1 and insulin-dependent

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

Secondary forms of DM

A

Pregnancy
Carbohydrate intolerance
Acromegaly
Cushing’s disease

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

Risk factors for DM

A

4-14y (peak 7-9y)
Females 2X as likely
Male neutered cats

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

General signs & symptoms of DM

A

Weight loss
PU/PD
Polyphagia
Glucosuria
Hyperglycaemia

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

Treatment of DM

A

Goal to eliminate clinical signs and resolve life-threatening hyperglycaemia & treat any concurrent disease
- insulin therapy (short or long acting)
- monitoring blood glucose and fructosamine levels
- dietary adjustment: high fibre, high complex carbohyrates, high protein
- glycaemic control: >80mg/dL
- exercise and weight loss

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

Why is a high fibre diet beneficial in DM patients?

A

Promotes weight loss and slows the absorption of glucose from the GIT which minimises the postprandial increase in glucose.

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

Somogyi effect

A

A too high administration of insulin results in periods of hypoglycaemia and rebound hyperglycaemia, release of glucagon, epinephrine, cortisol and GH. This results in an insulin resistance and a hyperglycaemia lasting 24-72h after a hypoglycaemic event

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

Treatment of somogyi effect

A

Decrease the insulin administration by 10-25%

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

DKA pathophysiology

A

Dysfunction of b-cells which result in absolute or relative deficiency of insulin. Insulin deficiency, diabetogenic hormone excess, fasting and dehydration lead to increased ketogenesis & gluconeogenesis. The liver is stimulated to produce glucose however cells are unable to utilise glucose due to a lack of insulin so fatty acids are converted into acetyl-CoA and further into the three ketone bodies: 1. Acetate, 2. acetoacetate, 3. b-hydroxybutyrate.
Diabetogenic hormone will enhance ketogenesis leading to ketonaemia and acidaemia.

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

Type of respiration associated with DKA or severe metabolic acidosis

A

Kussmal respiration

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

Risk factors and clinical signs of DKA

A

Diagnosed or undiagnosed DM
Dehydration
Weakness
Lethargy
Tachypnoea
Uraemic breath
Vomiting
Abdominal pain/distension
Plantigrade posture (cats)

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

Potential lab findings in patients with DKA

A

Severe uraemic acidosis (metabolic acidosis)
Lyte disturbances (K, Na, K, P)
Pre-renal azotaemia
Hyperlipidaemia
Haemoconcentration
Glucosuria, ketonuria, proteinuria
Ketonaemia
Leukocytosis
Increased liver and cholestatic enzymes

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

Potential ultrasound findings in DKA

A

Pancreatitis
Peritonitis
Hepatomegaly
UTI

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

Treatment of DKA

A

Main goals are to restore & maintain hydration, provide sufficient insulin, correct acidaemia & electrolytes, and treat underlying disorders.
IVFT: won’t decrease ketones but will reduce glucose and help correct dehydration
Insulin: usually regular insulin inititally after some time of rehydration
Electrolyte supplementation: K, Phos, Mg (if refractory hypokalaemia)
Bicarbonate: only if persistant pH <7
Glucose stabilisation & monitoring: reduce 50-100mg/dL/hr
Encourage eating: give anti-emetics etc as required

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

What cells make up the endocrine pancreas

A

a-cells: secrete glucagon
b-cells: secrete insuline
delta-cells: secrete somatostatin
f-cells: secrete pancreatic polypeptide
All regulate glucose production and utilisation

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

Hypoglycaemia signs

A

Lethargy
Ataxia
Coma
Weakness
Seizures/tremors
Death
Pupil dilation
Anxiety
Drooling

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

Neuroglycopaenia

A

Inadequate glucose concentration in the brain that affects the function of neurons altering brain function & behaviour.
(Severe neuronal damage -> reduction in ATP, cellular damage & oxidative damage)

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

Hyperosmolar hyperglycaemic state

A

Life-threatening emergency in patients with DM and is charatcerised by hyperglycaemia >600mg/dL and hyperosmolarity >350mOsmL, with dehydration and without a ketoacidosis.
Usually occurs when a DM patient stops drinking resulting in ongoing osmotic diuresis and PU resulting in significant free water deficit and increased osmolarity.

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

Serum osmolarity

A

(2 X (Na +K)) + (BUN/2.8) + (Glu/18)

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

Normal serum osmolarity for cats and dogs

A

Cats: 290-330
Dogs 290-310

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

Clinical signs of hyperosmolar hyperglycaemic state

A

Neuro signs
seizures
lethargy
weakness
hypothermia
anorexia
vomiting
death

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

Treatment of hyperosmolar hyperglycaemic state

A

Gradual rehydration 0.9% NaCl - replaces glucose with Na
Lower glucose to <250-300 by 50-75mg/dL/hr (not too rapid due to idiogenic osmoles)
Insulin therapy 0.025-0.05U/kg/hr (if too rapid drop in glucose drop insulin 25-50%
Address electrolytes (K, P, Mg)
Treat concurrent disease

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

Insulinoma….

A

Pancreatic b cell tumors that secrete insulin without regulation and are a type of amine precursor uptake & decarboxylation (APUD) -oma that are generally malignant.

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

Signs and symptoms of insulinoma

A

Hypoglycaemia
Weakness
Collapse
Weight loss

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

Treatment of insulinoma

A

Glucose administration (may be refractory)
Frequent meals (increased fat, fibre, carbs, AVOID simple sugars)
Glucocorticoids (glucagon 5-40ng/kg/min)
Ex-lap to remove tumor
Diazoxide
Somatostatin therapy (octreotide)
Prednisone

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

Hypoadrenocorticism pathophysiology

A

Inadequate secretion of glucocorticoids and mineralcorticoids by the adrenal cortex. It is usually due to bilateral adrenal atrophy with fibrosis and in most cases is immune-mediated. The primary mineralcorticoid which is deficient is aldosterone whilst the primary glucocorticoid deficient is cortisol & corticosterone.

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

Atypical Addison’s

A

Deficiency in ONLY glucocorticoid secretion

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

Cortisol

A

Regulates protein, carbohydrate and lipid metabolism, modulates immune function and ensures appropriate production of catecholamines

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

Aldosterone

A

Mineralcorticoid released from the Z. glomerulosa and part of the hormonal cascade that begins in the kidneys.
It also maintains normovolaemia and increased K excretion.

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

Signs & symptoms of hypoadrenocorticism

A

Weakness
Lethargy
Vomiting & diarrhoea
Weight loss
Anorexia
Trembling
PU/PD
Collapse
GI bleed

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

Signs of Addisonian crisis

A

Pallor
Tachycardia
Hypothermia
GI signs and haemorrhage
Hypoglycaemia
Hypotension
Hyperkalaemia

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

Risk factors for hypoadrenocorticism

A

Middle to old age
Female dogs
Std poodles, portugese water dogs, great danes, rottweiler, WHWT, wheaten terriers

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

Treatment of hypoadrenocorticism

A

Glucocorticoid therapy (hydrocortisone/pred/florinef/DOCP)
IVFT
Treatment of hypoglycaemia
Anti-emetics
GI protectants
Dexmethasone (won’t interfere with ACTH stim)
Treat underlying dz
Treat life-threatening bradyarrhythmia (due to high K)
AVOID nsaids

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

Lab findings with hypoadrenocorticism

A

ACTH stim
CBC: eosinophilia, NO stress leukogram
Blood smear: normocytic, normochromic anaemia
Biochem: pre-renal azotaemia & low albumin
Acid-base/electrolytes: metabolic acidosis, low Na + Cl, high K (Na:K <27:1), low glucose

57
Q

Glucose

A

The breakdown product of carbohydrates and is an important energy source in the animal body

58
Q

Glucose homeostasis

A

Balance between absorption, production & utilisation

59
Q

How does glucose become available

A

Via intestinal digestion and absorption of carbohydrates, the breakdown of glycogen via glycogenolysis or the production of glucose from gluconeogenesis

60
Q

Postprandial glucose is stored where as what?

A

Stored in the liver as glycogen.
Glycogen can be stored in any cell but mostly the liver and skeletal muscle

61
Q

Major hormones which regulate glucose

A

Insulin (released as BG rises)
Glucagon, catecholamines, cortisol & growth hormone (released as BG decreases)

62
Q

Glycogenolysis can sustain the body’s glucose demands for

A

6-12h

63
Q

Gluconeogenesis

A

Produces glucose in times of prolonged or increased demand and involves using end-products of glycosis i.e. lactic acid, pyruvate, glycerol and amino acids to produce glucose

64
Q

Cortisol role in glucose production

A

Helps to mobilise proteins and adipocytes to ensure amino acids and fatty acids are available for glucose production.
Also serves to inhibit the actions of insulin and potentiate effects of glucagon & epinephrine in the liver.

65
Q

What percentage of amino acids in the body can be converted to glucose

A

60%

66
Q

How much can the kidney contribute to total glucose production in circumstances such as hepatic insufficiency

A

40%

67
Q

Glucose transporters required for glucose to enter brain cells

A

GLU-1 TO GLU-5

68
Q

Treatment of hypoglycaemia

A

Buccal glucose limited effectiveness
IV Dextrose 50% 0.25-0.5g/kg dilute 1:3 (as req)
CRI IVFT + 2.5-7% D50
Glucocorticoids
Glucagon
Frequent meals
Monitor BG closely

69
Q

2 most common reasons for hyperglycaemia

A

Diabetes mellitus and stress-induced

70
Q

How does DM occur

A

Absolute or relative insulin insufficiency

71
Q

Other reasons for insulin deficiency excluding DM

A

exocrine pancreatic insufficiency, pancreatectomy

72
Q

Causes of hyperglycaemia

A

DM
Stress (catecholamine release)
Postprandial
Hyperadrenocorticism
Hypersomatotropism
Diestrus
Drugs (glucocorticoids, progestins)
Parenteral nutrtion
Fluids with glucose

73
Q

Glucosuria

A

Glucose is filtered by the kidney with almost all of it being reabsorbed into the PCT thus glucosuria rarer unless BG >180mg/dL in dogs and >300mg/dL in cats

74
Q

Clinical situations where insulin resistance occurs

A

Exocrine pancreatic insufficiency
Insulinoma
cortisol, epinephrine, GH or progesterone elevation (cushings, diestrus, high lipids, hypothyroidism)
Diabetogenic drugs

75
Q

Insulin resistance

A

exerts a negative influence on insulin sensitivity at the level of the insulin receptor or the insulin signaling cascade resulting in altered carbohydrate metabolism, increased hepatic glucose production, impaired peripheral glucose utilisation and relative insulin insufficiency.

76
Q

Adrenal cortex

A

Produce and secrete mineralcorticoids (glomerulosa), glucocorticoids (fasciculata) and sex hormones (reticularis) and are under the control of the juxtaglomerular apparatus.

77
Q

Adrenal medulla

A

Produces and secretes catecholamines and is regulated by the autonomic nervous system

78
Q

Pheochromocytoma

A

Catecholamine-producing tumors that predominantly arise from the adrenal medulla or extra-adrenal where they are neuroendocrine chromaffin cell tumors. They occur in 13-31% of all adrenal tumors.

79
Q

Pheochromocytoma pathophysiology

A

Intermittent production of supraphysiological catecholamines cause clinical signs associated with high sympathetic tone (tachycardia, arrhythmias, hypertension). As the tumor progresses intravacular invasion or thrombus formation and ascites may occur.

80
Q

3 layers of the adrenal cortex

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

80
Q

Pheochromocytoma clinical signs & PE

A

Weakness & collapse
PU/PD
Vomiting
Dyspnoea
Anorexia & weight loss
Seizures
Abdominal pain & ascites
Hypertensive crisis

81
Q

Treatment of pheochromocytoma

A

Treat hypovolaemic shock
Antiarrhythmics
Treat hypertensive crisis
Control excessive catecholamine release (phenocybenzamine, a-antagonist)
Adrenalectomy

82
Q

Hyperaldosteronism

A

Increased aldosterone either by increased autonomous secretion, decreased renal perfusion or excessive renin production.

83
Q

Primary hyperaldosteronism

A

Due to hyperplasia or neoplasia and is due to autonomous secretion. This is the predominant cause in cats.

84
Q

Treatment of hyperaldosteronism

A

Adrenalectomy (70-77% survival)

85
Q

Hyperadrenocorticism (cushings)

A

Excess adrenal cortex hormone release (most cases glucocorticoid excess). Most produced in the zona fascicula and reticularis under the control of the anterior pituitary with the release regulated by ACTH.

86
Q

Clinical signs of cushings

A

PU/PD
Polyphagia
Exercise intolerance
Muscle weakeness
Pot belly
Dermatological abnormalities (pyoderma, cutaneous atrophy)

87
Q

Amount of the adrenal cortex that must be destroyed before apparent clinical signs

A

90%

87
Q

Lab findings with hypercotisolism/hyperadrenocorticism/cushings

A

Thrombocytopathy
High ALP
High cholesterol
Hyperglycaemia
Low USG

87
Q

Where are the adrenal glands located

A

Craniomedial poles of the kidneys

87
Q

Treatment of hypercortisolism

A

Suppress glucocorticoid synthesis (trilostane)
Adrenalectomy (functional adrenal tumors)

87
Q

1 test for diagnosing cushings

A

LDDST. Can do urine cortisol:creanine ratio

88
Q

Most common form of hypoadrenocorticism

A

Primary, likely immune-mediated to all three layers of the adrenal cortex

89
Q

Secondary hypoadrenocorticism

A

Uncommon and results from abnormal pituitary or hypothalamic function (lack of CRH). Can occur due to trauma and neoplasia. Mineralocorticoid levels are preserved whilst cortisol production is affected.

90
Q

Aldosterone is vital to maintaining….

A

Normal sodium, potassium & water homeostasis at the site of the renal tubule. It also plays a role regulating the GIT as well as the salivary & sweat glands

91
Q

Aldosterone deficiency

A

Causes increased sodium, chloride and water via the urine contributing to dehydration, prerenal azotaemia, unconcentrated urine, hypovolaemia, weakness & shock.
It also impairs GI sodium absorption leading to decreased chloride and water absorption from the GI lumen.
Marked hyperkalaemia may also occur and is exacerbated by decreased GFR.
Acidosis also occurs and shifts K out of cells -> cardiac arrhythmias

92
Q

Glucocorticoid deficiency (low cortisol)

A

Leads to decreased intravascular volume, hypotension, and hypoglycaemia. Other: GI ileus, exacerbation of vomiting and diarrhoea.

93
Q

History & clinical signs of hypoadrenocorticism

A

Waxing and waning signs that are responsive to IVFT & glucocorticoid therapy, and are usually triggered by a stressful event. Extremely rare in cats.
Vomiting & diarrhoea
Melena
PU/PD
Ataxia
Tremors/seizures
Anorexia & weight loss

94
Q

Diagnosis of hypoadrenocorticism

A

Bilateral adrenal atrophy (can also be normal)
Microcardia, decreased pulmonary vessel vasculature, narrowed caudal vena cava (hypovolaemia)
Absence of a stress leukogram with variable WBC counts
Hyperkalaemia, low cholesterol, increased liver enzymes
Hyponatraemia (Na:K ratio <27:1; <20 VERY suggestive)
Azotaemia (prerenal) with inappropriate low USG
ACTH stimulation pre and post <2ug/dL (baseline cortisol <2ug/dL)
Hypoproteinaemia/hypoalbuminaemia
Hypercalcaemia
Metabolic acidosis

95
Q

Primary v. secondary hypoadrenocorticism

A

ACTH stimulation cannot differentiate. In the face of electrolyte abnormalities is highly probable that it is primary and mineralocorticoid therapy will be required long term. Where there isn’t electrolyte abnormalities it is hard to determine whether primary or secondary. Endogenous plasma ACTH will differentiate as will be high in primary due to loss of feedback inhibition from cortisol on pituitary function and low if secondary.

96
Q

Emergent treatment of hypoadrenocorticism

A

Shock: improve tissue perfusion, correct electrolytes, treat arrhythmias
Rapid IV glucocorticoids (dexamethasone or hydrocortisone)
Hyperkalaemia: mostly corrects with IVFT, calcium gluconate, dextrose, bicarbonate (if persistent low pH), tebutaline
* Cats can take 3-5 days before showing improvement

97
Q

Long term therapy for hypoadrenocorticism

A

Fludrocortisone (mineralcorticoid) + pred (for glucocorticoid)
DOCP (only mineralcorticoid) + pred

98
Q

Thyroid hormones

A

Critical in the regulation of physiological homeostatis: basal metabolic rate, many other body system functions.

99
Q

Thyroid hormone secretion

A

Relies on thyroid-stimulating hormone released from the posterior pituitary under negative feedback of T3 & T4

100
Q

Biologically active form of thyroid hormone

A

T3

101
Q

Thyroid testing

A

T4 the most sensitive indicator of thyroid dysfunction as 90% of EC pool of thyroid hormones is T4.

102
Q

Hyperthyroidism

A

Excessive thyroid hormone release and is mostly due to autonomous secretion due to hyperplasia or neoplasia.
Most common endocrinopathy of geriatric cats but rare in dogs

103
Q

Hypothyroidism

A

Inadequate thyroid hormone production and results from decreased TSH stimulation or decreased production of thyroxine within the thyroid gland. Most often due to immune-mediated destruction of the thyroid and is most common in dogs but quite rare in cats.

104
Q

Hyperthyroidism clinical signs

A

Reflect increased demands of excessive thyroid hormone
Polyphagia
PU/PD
Weight loss
Restlessness/altered behaviour
Vomiting & diarrhoea

105
Q

Diagnosis of hyperthyroidism

A

Suspicion
Elevated thyroid values
Enlarged thyroid

106
Q

Treatment of hyperthyroidism

A

Aimed at restoring normal thyroid hormone production
Methimazole
Iodide deficient diet
Thyroidectomy
Radioactive iodine deficiency

107
Q

Hypertensive retinopathy

A

Most common reason for acute blindness in geriatric cats and is often permanent so should be treated immediately. Cats will have mydriasis, retinal haemorrhage and hyphema. It is treatment with amlodipine and +- acepromazine or hydralazine.

108
Q

Thyroid storm

A

Rare consequence of uncontrolled hyperthyroidism and clinical signs reflect acute exacerbation of hyperthyroidism i.e. fever, cardiovascular, GIT and CNS signs. Treatment aims to decrease thyroid hormone production and decrease systemic effects of systemic thyroid hormones and identify underlying cause.

109
Q

Iatrogenic hyperthyroidism

A

Either by over supplementation or ingestion of thyroid-containing offal.

110
Q

Hypothyroidism clinical signs

A

Lethargy
Weight gain
Decreased appetite or stamina
Alopecia or ‘rat tail’
Seizures/vestibular disease
Stupor/coma

111
Q

Diagnosis of hypothyroidism

A

Low TT4
Mild, non-regenerative anaemia
Hyperlipidaemia

112
Q

Treatment of hypothyroidism

A

Levothyroxine

113
Q

Myxedema coma

A

Due to severe, untreated hypothyroidism leading to hyaluronic acid accumulation in the dermis leading to skin thickening, weakness, bradycardia, hypothermia, coma or death. It is treated with supplementating thyroid hormone, resuscitating the patient and quickly identifying underlying disease.

114
Q

Diabetes insipidus

A

Inadequate free water reabsorption in the kidneys causing polyuria. ADH is released from the posterior pituitary gland and acts on principal cells of the renal collecting tubules allowing electrolyte free water reabsorption in a normally water-impermeable region of the nephron. AVP/ADH released due to hyperosmolality or ineffective circulating volume and binds to V2 in renal collecting tubules activating G-protein and ultimately inserting specialised water channels into collecting tubule cell luminal membrane. They allow electrolyte free water to be reabsorbed from ultrafiltrate. Low AVP/ADH prevents this and large volumes of very dilute urine is produced, the animal drinks excessively to compensate.

115
Q

Nephrogenic v. central DI

A

Inadequate free water reabsorption in the kidneys causing polyuria. ADH is released from the posterior pituitary gland and acts on principal cells of the renal collecting tubules allowing electrolyte free water reabsorption in a normally water-impermeable region of the nephron. AVP/ADH released due to hyperosmolality or ineffective circulating volume and binds to V2 in renal collecting tubules activating G-protein and ultimately inserting specialised water channels into collecting tubule cell luminal membrane. They allow electrolyte free water to be reabsorbed from ultrafiltrate. Low AVP/ADH prevents this and large volumes of very dilute urine is produced, the animal drinks excessively to compensate.

116
Q

Nephrogenic v. central DI

A

Central due to pituitary disease and nephrogenic due to V2 receptor or aquaporin-2 channel issue.
Central: TBI, Neoplasia, pituitary surgery, ROSC, Inflammation, idiopathic, drugs
Nephrogenic: Paraneoplastic, hypercalcaemia, hypokalaemia, leptospirosis, ureteral obstruction, kidney failure, drugs

117
Q

Clinical signs of DI

A

PU/PD
Hypernatraemia
Inappropriately low USG (isosthenuric or hyposthenuric), isosmolar urine
CNS signs: seizures, head-pressing, obtundation

118
Q

Definitive diagnosis of DI

A

Exogenous AVP (desmopressin responsive >50% improvement in USG)
Modified water deprivation test (withhold water until 3% body weight loss, give exogenous AVP)

119
Q

Treatment of DI

A

Water replacement: D5W
AVP adminisatrion: desmopressin
* Must monitor Na and avoid too rapid drop to avoid cerebral oedema

120
Q

Acetyl-CoA synthesis

A

Either condensation or utilisation
Condensation: 2 ACA > acetoacetate > b-hydroxybutyrate and acetone
Utilisation: 3 ACA > acetoacetate > b-hydroxybutyrate and acetone

121
Q

Ketone bodies use

A

Synthesised as an alternative energy source when intercellular glucose concentrations cannot meet the metabolic demands. Acetyl-CoA produced from b oxidation of fatty acids which is facilitated by low insulin and increased glucagon

122
Q

Insulin protocols for DKA

A

0.2u/kg IM then 0.1u/kg IM one hour later
CRI 1.1-2.2U/kg/day

Add glucose to fluids to maintain BG, may need to adjust insulin CRI

123
Q

Pathophysiology of HHS

A

Increased circulating counter-regulatory hormones (glucagon, catecholamines, cortisol and GH) in conjunction with relative or absolute lack of insulin > inhibition of insulin mediated glucose uptake (epinephrine and glucagon) leads to glycogenolysis and gluconeogenesis; cortisol & GH inhibit insulin activity > increased circulating glucose.

124
Q

Diabetogenic hormones

A

Increased protein catabolism leading to impaired insulin activity and provides amino acids for hepatic gluconeogenesis

125
Q

Corrected Na

A

Na is the main determinant for serum osmolality and in a state of hyperglycaemia as seen in HHS will mask the true Na concentration, so corrected Na:

Na(meas) + 1.6 (glu(meas)-glu(norm)/100)

Glucose in mg/dL
Sodium mEq/L

126
Q

Glucagon

A

Secreted from pancreatic a-cells which stimulate the liver to perform glycogenolysis and gluconeogenesis to increase hepatic glucose production

127
Q

B-cells of the pancreas

A

Secrete insulin in response to increased glucose, amino acids and intestinal hormones. This stops glucose formation, promotes glycogen storage, stimulates glucose uptake and utilisation, decreases glucagon secretion and promotes triglyceride formation in adipose tissue

128
Q

Hypoglycaemia

A

Utilisation > production
1. Inadequate intake
2. Excessive utilisation
3. Dysfunctional glycogenolysis or gluconeogenic pathway

129
Q

SIADH

A

Syndrome of inappropriate antidiuretic hormone
Hyponatraemia due to excessive ADH release from the neurohypophysis or other source (cerebral, pulmonary or medication)

130
Q

Signs and findings of SIADH

A

Na <120mEq/L causing vomiting, CNS abnormalities, anorexia, arrhythmias. Osmolality usually <280mOsm/kg and urine osmolality >150mOsm/kg

131
Q

SIADH Treatment

A

Discontinue fluid therapy
Restricted water access
HTS3% over 2-4 hours
Reduce Na <12mEq/L/day
Initial Na aim 125-130mEq/L

132
Q

Low cortisol

A

Altered cellular function so affects; protein, lipid and carbohydrate metabolism, immunodysregulation, catecholamine & agremergic receptor function and dysfunctional cellular membranes > CIRCI

133
Q

Calculate osmolarity for a cat with Na 140, K 4.0, BUN 30, Glu 450

A

(2x(140+4)) + (30/2.8) + (450/18)
= 323mOsm/L (normal 290-330)

134
Q

Calculate osmolarity for a dog with Na 135, K 3.8, BUN 32.1, Glu 500

A

(2X(135+3.8)) + (32.1/2.8) + (500/18)
= 317mOsm/L (normal 290-310)

VTS(ECC) Preparation (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions