Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

4th year > SA Endocrinology > Flashcards

SA Endocrinology Flashcards

1
Q

Is more T3 or T4 produced by the thyroid gland? Difference between them? How are T3 and T4 transported? What form is active?

A

80% T4, 20% T3
But most T4 converted to T3 in peripheral tissues
T3 has more rapid onset of action and more potent than T4
>99% are bound to plasma proteins (TBG)
Only unbound thyroid hormone is active

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

Functions of thyroid hormones?

A

Increase the metabolic rate and O2 consumption of most tissues
Positive inotropic and chronotropic effects on the heart
Increase number and affinity of β-adrenergic receptors and enhance the response to catecholamines
Catabolic effects of muscular and adipose tissue
Stimulate erythropoiesis and regulate cholesterol synthesis and degradation

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

Canine hypothyroidism - Which dogs affected? Types?

A

Middle age-older dogs (large/giant breeds also when younger)

Congenital, acquired primary (most common) and acquired secondary

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

Congenital canine hypothyroidism - Cause? Presentation? Breeds affected?

A

Result of thyroid hypoplasia, aplasia or dyshormonogenesis
Disproportionate dwarfism
Fox and rat terriers (autosomal recessive)
Isolated TSH?TRH deficiency reported in a family of Giant Schnauzer and in a young boxer
Feature of panhypopituitarism in GSD
Rare!

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

What causes acquired primary canine hypothyroidism?

A

Immune condition - lymphocytic thyroiditis

Or idiopathic atrophy

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

What causes acquired secondary canine hypothyroidism?

A

Defect in the pituitary or hypothalamus

E.g. Aggressive pituitary neoplasia, treatment with high doses of potentiated sulphonamides

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

Clinical signs of canine hypothyroidism?

A 
Metabolic signs:
- lethargy
- obesity/weight gain
- exercise intolerance
- cold intolerance
Dermatological abnormalities:
- hair thinning or alopecia
- dry/poor coat quality
- skin hyperpigmentation
- pyoderma
- seborrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Haematology and biochemistry findings with Canine Hypothyroidism?

A

Low total T4, high TSH
Mild normocytic normochromic non regenerative anaemia
Hypercholesterolaemia
Hypertriglyceridaemia
Mild CK elevation
Mild ALP and ALT elevation
Elevation of circulating fructosamine (so don’t automatically think also diabetic! unless other positive signs/tests)

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

Total T4 (tT4) for canine hypothyroidism - Advantages? Disadvantages?

A

Cheap and readily available
More accurate than tT3 as doesn’t fluctuate as much throughout day
Sensitive
Not specific (tT4 is reduced in many non thyroidal illnesses and by many drugs) = many false positives if used alone
Greyhounds, other sighthounds and sled dogs have low normal values - use tT3

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

Free T4 (fT4) for canine hypothyroidism - How measured? Advantages? Disadvantages?

A

Measured by equilibrium dialysis
Usually normal in animals with low tT4 due to non thyroidal illness
less affected by presence of T4 autoantibodies
Good specificity
Lower sensitivity than tT4 = false negatives - especially early cases, affected by drugs
Expensive and not always available

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

TSH for canine hypothyroidism - High or low? Any problems?

A

High (loss of negative feedback)
Sometimes normal
Can also be high in non thyroidal illness and normal dogs
So use in combo with tT4

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

TgAAs for canine hypothyroidism - What do they indicate? Any problems?

A

Evidence of active immune reaction/inflammation
Approx 20% of dogs with TgAAs progress to thyroid dysfunction within 12mo
Cause aberrant test results (falsely elevated values of tT4 and tT3)
Approx 15% of hypothyroid dogs have T4 TgAAs - use fT4
Not the best diagnostic test so not used very often

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

What are the primary tests carried out for suspected canine hypothyroidism? Outcomes?

A

tT4 and TSH - outcomes:

  1. tT4 low, TSH high with compatible clinical signs = hypothyroidism
  2. tT4 and TSH normal = euthyroidism so end testing
  3. tT4 low, TSH normal = non thyroidal illness, previous drug therapy, or hypothyroidsm so need to test fT4 and TgAA
  4. tT4 normal, TSH high = compensating hypothyroidism, recent withdrawal from thyroid suppressive medication, recovery from non thyroidal illness, or T4 antibody interference so should repeat after loner periodd of drug withdrawal/recovery or perform fT4 and TgAA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do the outcomes of additional testing (fT4 and TgAA) for canine hypothyroidism mean?

A

Perform if tT4 low and TSH normal, or tT4 normal and TSH high

  1. fT4 normal and TgAA negative = hypothyroidism unlikely
  2. fT4 normal, TgAA positive = lymphocytic thyroiditis with solent or compensating hypothyroidism
  3. fT4 low and TgAA negative = hypothyroidism or severe non thyroidal illness
  4. fT4 low, TgAA positive = lymphocytic thyroiditis with hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment for Canine hypothyroidism? Monitoring? When should signs improve?

A

Levothyroxine
Care in cardiac patients - start at lower dose
Monitor tT4 4-6h post-pill (want to be in middle/top end of reference range)
Metabolic signs should resolve within first few weeks
Dermatological changes may take months

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

Feline hyperthyroidism - Cause?

A

98% due to nodular adenomatous hyperplasia (benign)
Usually bilateral
2% due to functional malignant tumours
Underlying causes - nutrition (canned food, liver, fish, giblet), environmental (indoor cats, using cat litter), genetic predisposition

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

Typical clinical signs of feline hyperthyroidism?

A

Weight loss despite polyphagia
PUPD
Hyperactivity
GI signs - V+D
Tachycardia, systolic heart murmur, gallop rhythm, arrhythmia, cardiac failure
Systemic hypertesnion
Skin and hair coat changes
<10% are ‘apathetic form’ - anorexia, depression, lethargy
In 80% of cases, enlargement of one or both thyroid lobes can be detected on palpation

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

Haematology and biochemistry findings for feline hyperthyroidism?

A 
Mild to moderate erythrocytosis and macrocytosis
Increased Heinz bodies
Increased mean lately size
Leucocytosis
Increased ALP, ALT, AST, LDH
Azotaemia
Hypokalaemia, hyperphosphataemia
Reduced fructosamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Total T4 (tT4) for feline hyperthyroidism? Advs and disadvs?

A

Most commonly used diagnostic test
Detects >90% of hyperthyroid cats
Used to monitor thyroid status in response to therapy
May not be elevated in early cases and when concurrent illness

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

Free T4 (fT4) for feline hyperthyroidism? Advs and disadvs? How measured?

A

Measured by equilibrium dialysis
More sensitive in early cases
False positives in cats with other illness
False positives are more common than with tT4

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

T3 suppression test for feline hyperthyroidism - How to do? Interpretation?

A

Collect basal bood sample for tT4 and tT3
Administer T3 orally every 8h for 7 doses (20ug if <5kg, 30ug if >5kg)
Collect second blood sample 2-6h after final dose for both tT4 (for diagnosis) and tT3 (to confirm tablets successfully given/absorbed)
Normal cats usually show at least 50% reduction in tT4 levels following suppression
Hyperthyroid cats generally show limited suppression

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

How does radionucelotide uptake and imaging (scintigraphy) work for feline hyperthyroidism?

A

Technetium-99m
Amount of fluorescing shown = allows identification of all hyper functional tissue
So if fluorescing more than salivary glands then is more active (abnormal)
Useful to show if ectopic thyroid tissue - thoracic inlet at base of heart (useful to know what to remove when planning surgery)

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

Medical management options for feline hyperthyroidism? Disadvantages? Adverse reactions?

A

Thiamazole/methamizole
- check tT4 after 2 weeks, then every 3 months
- now also available as a cream for trans-dermal absorption
Carbimazole
- slow release form in licensed
Both inhibit synthesis of thyroid hormone (blocks oxidation of iodine and coupling of iodothyronines to form T3 and T4)
Need owner and cat compliance
Rapid recurrence if medication missed
Adverse reactions
- anorexia
- lethargy
- vomiting
- pruritus
- haematological changes e.g. eosinophilia, lymphocytosis, leucopenia, agranulocytosis, thrombocytopenia
- hepatopathy
- acquired myasthenia gravis etc
B-adrenergic blockers and stable iodine to counteract the effects of thyroid hormone

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

Why may cats with hyperthyroidism and CKD have normal creatinine?

A

Muscle loss

Glomerular hyper filtration of creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Surgery for feline hyperthyroidism? Options? Pre-op management? Complications?
Thyroidectomy - unilateral or bilateral - staged or single - intracapsular or extracapsular Pre-op management - must manage medically for first 3-4 weeks - monitor biochemistry - hyperthyroidism increases GFR and can mask underlying CRF so consider reversible treatment if this is the case - thoracic radiographs to assess for evidence of CHF/pleural effusions - echocardiogram to assess systolic function Complications: - iatrogenic hypoparathyroidism -> hypocalcaemia - laryngeal paralysis - Horner's syndrome - recurrent laryngeal nerve damage resulting in voice change - hypothyroidism - recurrence of hyperthyroidism
26
Radioiodine for feline hyperthyroidism - how does it work? Advantages? Disadvantages?
Treatment of choice for permanent resolution Brachytherapy technique 131I preferentially concentrates in cells where there is upregulation of thyroid hormone production Concentrated very effectively in hyperplastic and adenomatous tissue 131I emits 80% β particles and γ rays β particles travel about 2mm in tissue (destroy the cells?) Treats any hyperfunctioning tissues Advs - permanent, no further treatment needed, no requirement for GA/surgery, up to 95% success rate Disadvs - expensive upfront cost, but poss cheaper than cumulative tablet cost, need cat isolation and facilities for disposal of radioactive litter etc, not widely available in UK
27
Non medical non surgical treatments of feline hyperthyroidism?
Percutaneous ethanol injection - only solitary nodules, side effects due to leakage of ethanol Hyperthermia - ultrasound guided heat ablation, transient responses, all cases recurred within 18mo Iodine restricted diet - difficult in multicat households (must be strict), not v palatable
28
Which part of the adrenal cortex secretes mineralocorticoids, glucocorticoids and androgens?
Zona reticularis: androgens Zona fasciculata: glucocorticoids Zona glomerulosa: mineralocorticoids? RFG AGM?
29
What are the effects of cortisol?
``` Facilitates: - gluconeogenesis - catabolism of fats to fatty acids and protein to amino acids - Na retention and H20 excretion - catecholamines -> vasoconstriction Inhibits: - uptake of glucose by muscle - ADH - bone resorption - calcium absorption in the intestine - collagen formation - protein synthesis - wund healing ```
30
Which animals get HAC?
Medium to older age dogs Very rare in cats (usually become diabetic first) PDH: more common in small breeds ADH: more common in large breeds
31
Common signs of cushings? And less common?
``` PUPD Polyphagia Panting Abdominal distension Endocrine alopecia Hepatomegaly Muscle weakness Systemic hypertension Less common: lethargy, hyper pigmentation, comedones, thin skin, poor hair regrowth, urine leakage, insulin resistant DM ```
32
Haematology, biochemistry and urinalysis findings of Cushings? Other general tests?
``` Haematology: - neutrophilic leucocytosis - lymphopenia - eusinopenia - thrombocytosis - mild erythrocytosis Serum biochemistry: - increased ALKP - increased ALT - hypercholesterolaemia - hypertriglyceridaemia - hyperglycaemia Urinalysis: - SG = 1.018-1.020 - proteinuria - UTI Reduced T4, normal TSH May see increased cPLI and snap PLI with no evidence of pancreatitis ```
33
Best screening test for Cushings? How does it work?
Low dose dexamethasone suppression test: - give dex - blood sample at 3 and 8h - avoid feeding during test - 85-100% se - 45-75% sp
34
ACTH stimulation test for cushings - how does it work?
``` Give ACTH Blood sample at 0 and 1h Avoid feeding during test Se 60% for AT, 80% for PDH Sp 60-90% Less effective screening test than low dose dex suppression test ```
35
Urine cortisol creatinine ratio for Cushings?
Random sample: - Se 75-100% - Sp 20-25% Sampling 2d after a clinic visit ie away from time of stress (2 samples both above cut off): - Se 94-100% - Sp 65-85% Used to rule out cushings (ie if negative, v unlikely to be cushings)
36
What does an adrenal panel test?
``` Baseline and post-ACTH Cortisol Progesterone 17-hydroxyprogesterone Oestradiol Androstenedione Testosterone ```
37
How to differentiate between PDA and FAT?
``` ACTH assay - normal reference range 20-100 - PDA >45 in 90% cases - FAT <20 in 70% cases Imaging High dose dexamethasone suppression test (not often used) ```
38
Treatment for cushings? Monitoring?
Trilostane - inhibits production of cortisol - other effects: adrenal necrosis, hypoadrenocorticism, lack of efficacy, V+D Monitor: - clinical signs - ACTH stimulation at 10-14d, or if dog well 3 months and repeat every 3 months for first year then every 6 months - single measure: pre-pill cortisol- if get hypertension (frequently occurs), treat with benazepril initially, amlodipine if refractory
39
Surgery for cushings?
Adrenal tumours - if not invading renal vein or vena cava, high morbidity at surgery but potentially curative Pituitary tumours - survival improving
40
Macroadenoma - What is it? Treatment?
Patient gets duller when treated but ACTH stimulation and metabolic screens are good Treat with hypophysectomy, radiotherapy
41
Which breed can look like they have cushings but actually have hepatopathy?
Scottish Terrier hepatopathy | Don't need trilostane!
42
Aetiology of hypoadrenocorticism?
Primary (Addison's): destruction of >90% of adrenal cortices - multiple autoimmune-associated genes may be involved Secondary: deficient ACTH (trauma, tumour) leading to atrophy go the adrenal cortex (primarily cortisol deficiency)
43
Which breeds are most commonly affected by hypoadrenocorticism?
Middle aged females Standard poodle, Beards, Great Dane, Portugese Water Dog, WHWT, St B, Wheaten terrier, Rottie, Leonberger Nova Scotia Duck-Tolling Retriever: 10x more common, affects siblings
44
Clinical signs for hypoadrenocorticism?
``` Vague malaise Vomiting (haematemesis) and diarrhoea/melaena Lethargy, weakness PUPD Abdominal pain Hypovolaemic collapse ```
45
Physical examination of dog with Addison's?
``` Weak pulses Increased CRT Dehydration Bradycardia Abdominal pain Collapse/syncope ```
46
Haematology and biochemistry of Addison's?
``` Mild non regenerative anaemia Mild hypercalcaemia Pre-renal azotaemia Lymphocytosis +/- eusinophilia Na:K ratio <27:1 Hyperkalaemia and hyponatraemia Isosthenuric to hypersthenuric urine Acidosis ```
47
'Atypical Addison's' - Presentation?
Cortisol deficiency Normal mineralocorticoids - usually progresses to deficiency Nor really atypical May have abnormal aldosterone stimulation - aldosterone receptors and renin-angiotensin increased
48
Differentials for hyperkalaemia, hyponatraemia?
``` GI disease Renal failure Parasitic infection (whipworms) Urinary obstruction Chronic effusion with repeated drainage Pregnancy CHF Diabetes mellitus Chronic blood loss ```
49
ECG changes that may be seen with Addison's?
``` Bradycardia Tall, narrow T waves Prolonged QRS interval Decreased P wave amplitude Prolonged P-R interval Absent P wave Complete heart block Ventricular arrhythmias ```
50
How does increasing hyperkalaemia with Addison's etc affect the heart?
>5.5mmol/l: peaking of the T wave and shortening of the QR interval >6.5mmol/l: increased QRS duration >7mmol/l: decreased P wave amplitude, prolonged PR interval >8.5mmol/l: absent P wave and severe bradycardia
51
Testing for Addison's?
``` Single cortisol - if normal, rules out Addison's <55nmol/l has 100% se, 63% sp Pre and post ACTH: - pre ref 20-250 - post ref 20-450 ```
52
Electrolytes, pre-ACTh cortisol, post-ACTH cortisol, endogenous ACTH, cortisol:ACTH and Aldosterone:renin for primary, atypical primary and secondary hypoadrenocorticism?
Electrolytes - abnormal for primary, normal for atypical primary and secondary Pre and post ACTH cortisol - low for all 3 Endogenous ACTH - high for both primaries, low for secondary Cortisol:ACTH - low for both primaries, high for secondary Aldosterone:renin - low for both primaries, normal for secondary
53
Treatment for hypoadrenocorticism?
Fluid therapy: - 0.9% NaCl shock rate initially (60-80ml/kg/hr) - NB rapid changes in Na can cause problems later (myelinosis) - don't increase Na more than 0.5mmol/l/hr - monitor CRT, BP, lactate, base excess, urine output Treat the hyperkaelaemia: - soluble insulin IV - dextrose in IV fluids - calcium glutinate 10% IV - monitor glucose and K Steroids - dexamethasone sodium phosphate - hydrocortisone - predinosolone sodium succinate - oral prep or fludrocortisone once eating - maintenance therapy: oral pred may only be needed at times of stress, fludrocortisone - DOCP
54
Risks with hypoadrenocorticism treatment?
Acute renal failure Myelinosis - depression, weakness, ataxia, tetraparesis, decreased sensory perception Signs occur days later and often irreversible
55
Phaeochromocytoma - signs? diagnosis? treatment?
= tumour of adrenal medulla secreting catecholamines Anxiety, tachycardia, tachypnoea, V+D, weight loss, hypertension (retinal detachment) Diagnosis: radical excision (high risk), antihypertensive medication Frequently metastasise
56
Hyperaldosteronism - cause? signs? treatment?
Adrenal tumour producing aldosterone Not reported in dogs PUPD, weakness, neck ventroflexion (hypokalaemia), hypertension (Na retention) Treatment: restrict Na and supplement K, surgical excision, spironolactone
57
Aetiology of DM in dogs?
``` Loss of islets: - infection - pancreatitis - immune mediated disease - hormonal/drug antagonsim Predisposing: - obesity - endocrinopathy - hyperlipidaemia ```
58
Aetiology of DM in cats?
``` Type 2 like insulin resistance +/- relative insulin deficiency Predisosing: - obesity - GH excess -> beta cell exhaustion (glucotoxicity) Type 1 is uncommon: - amyloid deposition - pancreatitis - neoplasia ```
59
What happens as a result of insulin deficiency?
``` Increased glucagon Increased gluconeogenesis Decreased cellular uptake Osmotic diuresis Fatty acid mobilisation -> ketoacid production ```
60
Clinical signs of DM?
PUPDPP | Weight loss
61
Biochemistry and urinalysis findings of DM?
``` Hyperglycaemia Elevated ALT and ALKP Hypertriglyceridaemia Low USG Glycosuria Ketonuria Active sediment ```
62
Criteria for diagnosing DM?
Appropriate clinical signs + persistent fasting hyperglycaemia + glycosuria
63
Treatment of DM?
Dogs - lifelong twice daily insulin, feed half ration and then administer insulin, high fibre/complex CHO diet Cats - may go into remission (monitor as can become hypoglycaemic), twice daily insulin, low CHO/high protein diet Short acting insulin: regular crystalline Intermediate acting: caninsulin (licensed) Long acting: prozinc (licensed) Oral hypoglycaemic drugs - sulfonylureas (not first choice) Caloric intake, consistent feeding, consistent exercise
64
How to monitor a diabetic dog or cat?
Clinical signs - thirst, appetite, weight gain Urine glucose - afternoon sample, don't adjust insulin based on this Glucose curve - NB 5-7d for adaptation Fructosamine
65
Signs of insulin overdose? Treatment of hypoglycaemia? What to do if not eating?
``` Ataxia, collapse, seizure Give sugary substance under tongue Feed ASAP Avoid insulin dose if imminent If not eating, reduce insulin dose by 50% (do not stop insulin) - basal insulin always needed to control glucose entry into cells ```
66
Glucose curves - how does it work?
Duplicate diet and timing Serial blood samples - patient side monitor Sample every 2h Nadir should be between 4.5-9mM Twice daily insulin: - if not returned to >9mM by 12h - do not inject insulin - feed and continue monitoring until reaches >14mM to assess duration of action of insulin Wireless monitoring with interstitial fluid monitor - record every 2 mins to 2 days, usually stop working in 7-14d
67
Problems with serial blood glucose curves?
Activity level Poor appetite Stress
68
Causes of recurrence of DM clinical signs?
Administration technique and insulin activity problems Insulin overdose and glucose counter-regulation Short duration of insulin effect Inadequate insulin absorption Circulating insulin binding antibodies Concurrent disorders causing insulin resistance
69
Chronic complications of DM?
``` Ketoacidosis Infections Lens induced uveitis Diabetes neuropathy Cataracts Diabetic retinopathy ```
70
Measuring BID glucose insulin curve duration?
Time from injection past nadir back to 13mM or to 70% of basal level
71
If glucose curve shows animal not responding to insulin, what should you do?
<2IU/kg -> increase dose | >2IU/kg -> insulin resistance? - UTI, other diseases, insulin autoantibodies?
72
If glucose curve shows nadir too high or low, what should you do?
<4mmol/L -> decrease insulin dose | >8-9mmol/L -> increase insulin dose
73
What to do if glucose curve shows nadir right level (4-8mmol/L) but still showing clinical signs?
May be too short duration -> consider longer acting insulin
74
Why may there be an overswing seen on a glucose curve with DM?
Counter-regulatory hormones (glucagon, epinephrine, cortisol)
75
Aetiology of diabetic ketoacidosis? Clinical signs? Diagnosis?
``` Insulin deficiency Insulin resistance Increased circulating levels of diabetogenic hormones Signs: - vomiting - depression - dehydration - weakness - tachypnoea - signs of concurrent disease e.g. pancreatitis Diagnosis: diabetes + ketonuria ```
76
Treatment for diabetic ketoacidosis?
``` Provide adequate amounts of insulin Restore water and electrolyte losses Correct acidosis Identify any concurrent illness Provide carbohydrate substrate Treat if sick patient/V+D/malaise -> hospitalise (outpatient if well in self) Potassium supplementation Phosphate supplementation Bicarbonate therapy Insulin therapy Fluid therapy ```
77
Normal feline thyroid anatomy - Size? Location? What if enlarged?
1cm long, 3-5mm wide, 1-2mm thick Lateral and sometimes slightly ventral to the trachea Enlarged glands tend to migrate caudally into the lower cervial/thoracic inlet
78
Feline parathyroid gland anatomy - Shape? Size? Location?
Two round flat glands Associated with each thyroid galnd 4mm diameter Location varies lots! Cranial/external - white, attached to transparent capsule, near the cranial pole Internal - caudal half of the thyroid parenchyma, not visible to surgeon
79
Feline thyroidectomy - Method of exposing thyroid glands? Deciding whether to do unilateral or bilateral?
Extend neck - avoid any rotation Ventral midline skin incision from larynx to cranial aspect of manubrium Elongate over manubrium for caudally displaced glands Bluntly separate the sternohyoideus muscles along the midline raphe Separate the sternothyroid muscles more laterally and deep Retract the above muscles to expose the trachea The thyroid glands are found in the lateral paratracheal fascia Normal thyroid = pale tan, adenomas are typically brown to red brown Check both thyroids If unilateral disease, the normal gland will atrophied If both large or one large, one small then probably both abnormal Identify parathyroid glands If bilateral, operate on side with the more easily identifiable and so more easily preserved parathyroid gland first
80
Feline thyroidectomy techniques? Which to use?
Extracapsular thyroidectomy = intact thyroid removed with capsule, no attempt to preserve external parathyroid gland (low recurrence but hypoCa) Intracapsular thyroidectomy = incision into thyroid capsule, capsule left to preserve cranial PT (increased recurrence but low hypoCa) Modified extracapsular thyroidectomy = thyroid capsule incised around cranial parathyroid gland and separated from thyroid gland, preserves cranial thyroid artery to PT, remaining thyroid gland with capsule is removed (low recurrence, 23% hypoCa) Modified intracapsular thyroidectomy = incision made in ventral capsule of thyroid gland, thyroid gland dissection, cranial PT gland and blood vessels preserved (low recurrence, 36% hypoCa) Modified techniques are recommended Staged techniques not shown to have any advantage
81
What to do if you damage the parathyroid gland blood supply during a feline thyroidectomy?
Be more careful to preserve the PT blood supply on the other side Or can do PT autotransplantation - place in muscles of sternothyroideus/sternohyoideus - revascularisation -> functioning in 7-21 days -> still can get acute hypoCa but will offset longterm Ca supplementation
82
Signs of post-operative hypocalcaemia from a feline thyroidectomy?
``` Signs usually occur 1-3d post-op but can be 12h-6d post-op Restlessness Facial or generalised muscle twitching Weakness Lethargy Anorexia Seizures Ataxia Tachycardia, weak pulses Anxiety ```
83
What should you do to check for hypoCa for a feline bilateral thyroidectomy? Treatment if hypoCa?
Measure ionised Ca before surgery and 18-24h post-op If acute signs of hypoCa: give 10% calcium gluconate Administer CRI of calcium gluconate - monitor for bradycardia and arrhythmias Once stable, administer oral vit D and Ca If did PT autotransplantation, hypoCa usually resolves in 3 weeks Without, can last up to 4 months
84
Primary hyperparathyroidism - aetiology? clinical signs? diagnosis? Treatment?
``` Most nodules in dogs are adenoma, up to 5% are carcinomas Functional tumur producing PTH HyperCa -> - PUPD - urolithiasis (stranguria, pollakuria, haematuria) - cystitis - dehydration - dystrophic calcification - renal damage (AKI) Lethargy Fibrous osteodystrophy (rubber jaw) Diagnosis: high total Ca and iCa, normal to low PO4, high PTH, detect mass in thyroid/parathyroid area Ultrasonography Keeshond breed most at risk Treatment: restore normal calcium level by - fluids (0.9% NaCl) - frusemide (after rehydration) - prednisolone - calcitonin - biphosphates - surgical removal of tumour ```
85
Method for parathyroidectomy?
Ventral midline cervical approach from the larynx to the manubrium Delicate surgery – requiring fine instruments and bipolar cautery Correctly identifying abnormal glands can be difficult Cranial PT – can be dissected from thyroid gland Caudal PT – partial thyroidectomy; guillotine technique
86
How to manage cats post-parathyroidectomy?
Up to 70% develop hypoCa ICU - keep quiet, don't allow to over exercise May need supplementeation If over-supplement, other PT gland are unlikely to respond and start functioning But if not supplementing can lead to hypoCa tetany Difficult to get right - can take months to get stable
87
Canine thyroid carcinoma - prevalence? functional? breeds affected? Signs?
``` At necropsy 50% adenomas 90% of clinically detected thyroid tumors are carcinomas 40 – 80% metastatic rate 30% HyperT4 10% HypoT4 60% Euthyroid Older large breeds Most common sign is mass palpable on ventral cervical area ```
88
Complications of canine thyroidectomy for a carcinoma?
Can be moveable and amenable to surgical excision or fixed and very invasive Can include: - Jugular vein - Carotid artery - Vagosympathetic trunk - Recurrent laryngeal nerve Complications: - haemorrhage (significant) - hypoT4 - laryngeal paralyisis - megaoeophagus - hypoPTH (bilateral)
89
Canine adrenalectomy - When performed? Method?
Treatment of choice if malignant adrenal carcinoma but hasn't metastasised Not indicated for small, benign hormonal inactive masses Adrenal glands are retroperitoneal Ventral midline approach Often very vascular Some of these tumours may invade caudal vena cava requiring a venotomy - need specialist referral
90
Complications of canine adrenalectomy?
Common and most are life threatening Haemorrhage Pulmonary Thromboembolism Hypoadrenocorticism Surges of catecholamine release when handling phaeochromocytomas: hypertension, ventricular tachycardia, arrhythmias
91
Differentials of PUPD?
``` Primary diabetes insipidus - rare Central diabetes insipidus - rare Secondary diabetes insipidus - pyometra - renal failure - hyperCa - cushings - hyperthyroidism - pyelonephritis - Addison's - liver failure - hypokalaemia - acromegaly Osmotic diuresis - DM - primary renal glucosuria - Fanconi's syndrome - post-obstructive diuresis Iatrogenic - glucorticoids - diuretics - phenobarbitone - high salt diet - levothyroxine - vitamin D toxicity Renal medullary washout (loss of hypertonicity of medulla due to long term PUPD) Primary polydipsia - problem of thirst centre in brain - psychogenic or behavioural ```
92
Definition of PD?
>100ml/kg/day
93
Initial work up for PUPD?
History (rule out iatrogenic) Physical examination (evidence of renal disease, pyometra etc) Haematology (evidence of pyometra/pyelonephritis) Biochemistry (hypoNa? Renal disease? Diabetes? Bile acids (liver disease) T4 (hyperthyroidism?) Urinalysis (diabetes? Faconi's? Renal glycosuria? Culture to rule out pyelonephritis/UTI) Should then have diagnosis If not then: - HAC - Central DI - Primary NDI - Primary polydipsia Next step = rule out HAC Final step = water deprivation test, followed by response to exogenous DDAVP (to differentiate CDI, primary NDI and primary polydipsia)
94
Treatment of Central Diabetes Inspidus (CDI)
DDAVP nasal drops applied into conjunctiva 1-4 drops once/twice daily Titrate to clinical signs
95
Differentials for poor growth?
Nutritional - e.g. underfeeding Physiological - e.g. breed size variation GI - parasites, megaoesophagus, vascular ring anomaly, chronic GI obstruction, EPI Cardiac - congenital heart disease, endocarditis Renal - renal dysplasia, polycystic renal disease, tubular defects Liver - portosystemic shunt, hepatitis Lysosomal storage diseases Endocrine: - GH deficiency - hypothyroidism - hypoadrenocorticism - HAC - DM - Rare pituitary endocrinopathies (pituitary dwarfism, acromegaly, diabetes inspires) - hyper/hypoparathyroidism
96
What does the anterior and posterior pituitary produce?
Anterior - FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH | Posterior - oxytocin, ADH
97
Pituitary dwarfism - Breeds affected? What happens? Clinical signs? Diagnosis?
``` Rare congenital lesion Almost exclusively GSDs Failure of GH secretion +/- FSH, LH, TSH Proportionate dwarfism: - failure to develop adult coat - delayed dental eruption - delayed growth plate closure - thin, fragile, hyper pigmented skin - pyoderma - immature glands Rule out other causes of retarded growth Definitive diagnosis: dynamic test to assay GH (impractical), IGF-1 ```
98
Treatment for pituitary dwarfism?
Progestagens - induce GH secretion from mammary tissue GH - results usually disappointing, skin signs may improve Check thyroid status (supplement if needed) Do not breed
99
Acromegaly - What is it? Which animals affected? Aetiology? What happens? Diagnosis? Treatment?
Chronic excess GH Cats: pituitary tumour, older males Dogs: mammary tissue in response to progesterone/progestogens, intact females/females receiving progestagens Results in insulin antagonism causing insulin resistant DM and anabolic effects from IGF-1 = excessive growth of extremities, prognathism, wide interdental spaces, soft tissue proliferation, insulin resistant DM Diagnosis: DM, liver enzyme elevation, elevated IGF-1, MRI/CT Bitch treatment - OVH or stop progestagens, bony changes irreversible Cat treatment - attempt to control DM, surgery (hypophysectomy), radiation of pituitary mass
100
Forms of secondary hyperparathyroidism?
Renal secondary hyperparathyroidism | Nutritional secondary hyperparathyroidism
101
What is pseudo-hyperparathyroidism?
Caused by a tumour secreting PTH-rp
102
Types of hypoparathyroidism? Signs? Diagnosis? Treatment?
``` Primary (immune mediated) Secondary (surgery) Signs of hypocalcaemia Diagnosis: low Ca, high PO4, low PTH Emergency: - IV fluids - IV/SC calcium gluconate (slow, ECG) Maintenance: - oral calcium and Vit D ```
103
Causes of low Ca2+?
``` Hypoparathyroidism CKD Puerperal tetany AKI Acute pancreatitis ```
104
Insulinoma - What is it? Clinical signs? Diagnosis? Treatment?
Functional tumour of pancreatic B-cells producing insulin -> hypoglycaemia Often episodic (fasting, exercise, excitement) Weakness, trembling, ataxia, seizures +/- other neurological signs May have weight gain Diagnosis: - persistent hypoglycaemia (but normal does not exclude) - elevated insulin (fast until patient is hypoglycaemic then measure insulin = normal or high in insulinoma) - pancreatic mass Treatment: - IV glucose if needed - give small frequent meals, avoid simple sugars, use diet high in complex carbs, protein and fat (to avoid excess stimulation of insulin) - prednisolone - oral hyperglycaemic (expensive, not licensed) - surgery
105
Gastrinoma - What is it? Problems? Diagnosis? Treatment?
Rare Pancreatic gastrin-producing tumour Gastric hyperacidity and risk of ulceration GI signs can be very severe Diagnosis: elevated gastrin levels, imaging, endoscopy Can be surgically removed but frequent metastases

4th year (44 decks)

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