Term 5 Week 7 Endocrine

What type of hyperglycemia is seen in dogs with DM helps in the diagnosis

Concurrent persistent hyperglycemia + glucosuria, usually with CS establishes diabetes

A 10 year old cat has weight loss and PUPD. Hospital BG is 320mg/dL with 2+ glucosuria, but the cat was extremely distressed. What is the best next step?

Confirm sustained hyperglycemia

What type of hyperglycemia is seen in cats with DM helps in the diagnosis

Prove sustained hyperglycemia, stress produce marked hyperglycemia and glucosuria use at home non stressed glucose or glucosuria, fructosamine or another glycated marker interpreted with its limitation

Transient hyperglycemia is less problematic in which species

In dogs than in cats (in dogs

What can you do to dx DM in dogs and cats

Dogs: concurrent hyperglycemia + glucosuria

Cats: prove persistence

What can you use to stage DM

Ketones/BHB, electrolytes, hydration and acid base status

Look for concurrent dz

What is the best use for BG and DM and its limitations

Use: current glucose; curves hypoglycemia

Limits: spot values do not describe duration or variability

What is the best use for UA and DM and its limitations

Use: glucosuria, ketonuria, infection clues

Limitation: reflects time since last void; poor dose adjustment tool

What is the best use for blood BHB and DM and its limitations

Use: earlier, quantitive assessment of ketosis

Limitation: interpret with clinical status and tx type

What is the best use for fructosamine and DM and its limitations

Use: average glycemia over 7-10 days, trend monitoring

Limitation: affected by protein turnover/concentration; misses brief excursions

What is the best use for CGM and DM and its limitations

Use: multi-day pattern, nocturnal lows, home routine

Limitation: interstitial lag and reduced accuracy at low values

What is the best use for HbA1c and DM and its limitations

Use: potential 2-3 months average

Limitation: commercial vet assays not yet validated in diabetic dogs/cats

How do you confirm DM in cats

Increased fructosamine

Repeat BG or glucosuria at home/non-stressed

CGM or vet calibrated PBGM

Avoid dx from one stressed sample

If at home urine is the only option aim for home many samples on different days after stress of first visit has resolved

>2 samples

What value of blood BHB indicates ketosis

> 1.0 mmol/L

What will impair control of DM in dogs

Urine culture when infection is suspected or risk is high

Review glucocorticoids/progestogens

Consider pancreatitis, hyperadrenocorticism and diestrus

Assess cataracts, neuropathy and body weight

What will impair control of DM in cats

TT4 and BO

Assess CKD, pancreatitis, dental dz and infection

Consider hypersomatotrophism or hyperadrenocorticism when indicated

Record body and muscle condition score

When can you monitor DM tx

Baseline: signs, weight, dose, diet, choose home monitoring plan

5-14 days (early recheck): after insulin starts or any dose change, assess nadir and duration

Any time (loss of control): recurrent signs, suspected hypoglycemia, illness or weight loss

Stable (periodic review): clinical log, weight, minimum database and fructosamine as appropriate

What is NADIR

The lowest point that glucose curve goes after insulin administration (typical feline target: 80-150mg/dL)

The duration of insulin means what

How long the insulin was about to manage the BG

Dogs: 80-200

Cats: 80-300

Why is CGM beneficial

Reading across several days- can review trends

Overnight and unobserved hypoglycemia

Response to meals, treats and exercise

Data from the home environment

How long is the interstitial to blood lag

5-15 min

What is the half life of albumin

2-3 weeks

When is fructosamine a useful test

Following change over time

Supporting the overall clinical impression

Flagging possible chronic hypoglycemia when below reference interval

Monitoring stable patients when CGM/BGC is impractical

Why can fructosamine readings be misleading

Protein loss, altered albumin turnover and hyperthyroidism can lower results

Brief hypo or hyperglycemic episodes can be missed

Can urine glucose safely direct insulin dosing

NO it does not define the NADIR, duration or current blood glucose if only tells you if glucose was over threshold (we don’t know for how long or how high and we also don’t know how low if it is under threshold)

What is the renal threshold for glucose in dogs and cats

Dogs: 160-200 mg/dL

Cats: 250-300 mg/dL

An insulin treated cat is clinically improved. A home curve shows a NADIR of 48 mg/dL; all other values are 95-260 mg/dL. What is the best action?

Decrease the insulin dose because hypoglycemia occurred

What is BHB

Beta-hydroxybutyrate

If a cat is being given SGLT2i what MUST you monitor

Blood BHB (during the first 2 weeks ketosis surveillance matters more than a glucose curve)

A sick cat receiving an SGLT2i inhibitor should be treated as what type of risk

Ketotic/DKA risk even if glucose not markedly high

What is the schedule for monitoring a cat is being given SGLT2i

Before tx: eating, hydrated, clinically stable, CBC, chem, UA, BHB

Days 2-3 and 7: history, examination and weight/hydration, repeat BHB; investigate poor appetite, vomiting or lethargy

Day 14 → 30 → q3 months: BHB + clinical status + weight, BG, fructosamine by day 30 as indicated

If you have signs of controlled DM and occasional BG >300 what is you next step

May still be acceptable, especially in dogs, do not increase dose from this alone

If you have a low BG at any point what is you next step

Insulin dose may be excessive, reduce dose, confirm safety and feeding history

If signs of DM persist and NADIR is acceptable what is your next step

Duration may be too short, review curve/CGM and insulin choice

If you have high fructosamine and a clinically well animal what is your next step

Marker and clinical status conflict, review trend, protein status and glucose pattern

If you have unexpected poor control of DM what is you next step

Administration or concurrent disease possible, observe technique, verify insulin, investigate resistance

A cat receiving an SGLT2i for 5 days develops vomiting and lethargy. BG is 160 mg/dL. What is the most important immediate next step?

Measure blood BHB and assess for euglycemic DKA

A defensible monitoring plan for DM triangulates what four signals

Patient: clinical signs, appetite, behavior, body weight and condition

Tx: insulin/SGLT2i dose, timing, handling, administration and diet

Glucose pattern: home BGC or CGM when a tx decision requires it

Complementary test: fructosamine trend, UA, BHB, and min database

Can you dx cats with DM from one stressed sample

NO

You are not supposed to make insulin doses based on what

Spot glucose (anything outside the NADIR)

What can owners monitor at home

Attitude (hypoglycemia will see pylatism)

Appetite (should be hungry if not eating something else is going on)

Water intake and PU (have owner measure amount they are giving)

Body weight (stand on scale with cat and without cat)

Urine glucose (not sensitive but monitoring trends can help and changes should necessitate a visit to your clinic)

Serum or urine ketone (with SGLT2i)

Glucometer (using the marginal ear vein)

FreeStyle Libre 2 (good for monitoring hyper and euglycemia, overestimates glucose in HYPOglycemia)

Owners should consult you before changing dose (you make changed based on curves/average daily glucose and CS)

Which type of DM cannot be put on SGLT2i

Type 1 (they need insulin!!!)

In which animals should you not put on SGLT2i

Animals that have been on insulin

What does free style Libre test

Interstitial glucose

What are some long term additional monitoring tools you can use in a DM animal

Clinical signs

Recheck every 2-4 months

Fructosamine levels (should glucose over 2-3 weeks)

Used more commonly as we increase SGLT2i use

Why are vets afraid of hypoglycemia

Animals die from this

What are some behavioral changes associated with hypoglycemia

Ataxia

Depression

Ptyalism

(your must tell owners to look out for these)

What are causes to hypoglycemia

Insulin overdose

Incorrect syringe

Insulin given to anorexic animal/vomiting (owners can ½ insulin but must bring them to the clinic as well)

Long-acting insulin

Cat who requires only 24hr dosing (glargine)

Aging (can go from type 2 to type 1)

Adrenalectomy

Beta blockers

Remission (sometimes diet alone can can lead to remission)

What can owners give to hypoglycemic pets

Karo syrup on the gums

What are some complications that can be seen with DM

Chronic infections (UTI and dermatologic)

Monitor often, culture always and tx aggressively

Hepatic lipidosis (common 2 dz)

Iatrogenic hypoglycemia

Ketoacidosis

Neuropathy (plantar stance more common in cats than dogs)

Persistent CS (once given insulin should decrease)

Diarrhea

EPI

Gastric paresis

Glomerulonephropathy

What are some surgeries that may be requested in animals with DM

Cataracts (acute blindness) and spays (preg or diestrus associated)

What must you do in an animal going to surgery with DM

Only do if procedure necessary

Ensure good glycemic control

No food in AM so ½ dose of insulin

Schedule procedure first

Monitor frequently

5% dextrose in fluids

Can use regular insulin until awake enough to eat then back to SQ

How long can it take to reach a steady state with DM tx

5-7 days

Will animals be good on q24hr insulin

Only 5-10% of dogs

START WITH BID

How much should you adjust insulin dose

10-15% and reassess in 5-7 days

How will I know if a cat is insulin resistant

If not responsive with an insulin dose of >2U/kg (they either could have incorrect insulin handling or administration and concurrent dz)

What should you assess for if an animal is insulin resistant

Ensure owner compliance

Medications: steroids

Insulin: appearance, storage, handling, syringes and practice

Concurrent dz: dogs (hyperadrenocorticism, hypothryoidism, chronic pancreatitis) and cats (acromegaly, hyperthyroidism, hyperadrenocorticism)

Fear (epinephrine)

What is the somogyi effect

If the body has severe hypoglycemia you will see a rebound hyperglycemia because hypoglycemia turns on anti-insulin hormones

What will owners notice with the somogyi effect

A return of CS

Glycosuria, spot BG measurement showing severe hyperglycemia

A previously well controlled DM patient is reported to have a return of CS and inappetent. What are you concerns

Another dz is going on (they should NOT be inappetent)

What are some other dz you are concerned about with DM

Infection (upper UTI will be sick but not from bladder infection) ALWAYS culture

Acromegaly (25-28% of DM cats have this)

Hyperadrenocorticism

Is an animal sick with a bladder infection

NO just in pain

If a cat has HAC they automatically have what

DM

In dogs with HAC do they have DM

Can have concurrently BUT HAC is not reason for their DM (unlike cats)

Should a controlled DM dog be sick

NO

What is acromegaly

GH excess

Which cats usually get acromegaly and what normally causes it

Older cats (MALES)

GH secreting tumor (90% macroadenoma)

Will have insulin resistance

Which dogs usually get acromegaly and what normally causes it

Older intact females with transient diestrus causing GH production in mammary glands

What are CS of acromegaly

PUPD

Polydipsia

Polypagia (can be extreme)

Weight gain (could start with loss)

Stridor

Broad freatures

Prognathia inferior

Abdominal enlargement

Clubbed paws

Neurologic sings (brain tumor)

What is a unique sign of acromegaly

Weight gain

Why do animals with acromegaly get stridor

Face is growing- elongated soft pallet

What is the difference between prognathia and brachygnathia

Prognathia (prognathism) refers to a jaw that abnormally protrudes forward, whereas brachygnathia (brachygnathism) refers to a jaw that is abnormally shortened

How can you diagnose acromegaly

Bloodwork: hyperproteinemia, hyperglycemia, glucosuria

CT/MRI (look for tumor)

IGF-1 levels (initial and monitor every 1-3 months)

Why do you test IGF1 for acromegaly

• Excess GH stimulates the liver and other tissues to produce abnormally high levels of IGF-1.

• The Effects: Elevated IGF-1 drives the progressive enlargement of bones, soft tissues, facial features, hands, feet, and internal organs

What combination points to acromegaly

DM

Renal dz

Cardiomyopathy

Stridor

Conformational changes

What is the tx for acromegaly in dogs

Spay

What is the tx for acromegaly in cats

Pituitary dz: radiation therapy will recur in 12-24 months

Surgery: hypophysectomy (85% of DM will not need insulin with this)

Cabergoline or pasireotide

List the anti-insulin hormones

Glucagon, progesterone, cortisol, epinephrine, GH

What will you see on CBC with hypothyroidism

Mild normocytic, normochromic, non-regenerative anemia (25–40%) +/- Increased WBC count - Often due to infection (e.g., pyoderma)

What will you see with erythrocyte morphology with hypothyroidism

Target cells (leptocytes) - Associated with altered lipid metabolism

What will you see on chemistry with hypothyroidism

Hyperlipidemia: Increased triglycerides and fasting hypercholesterolemia (>1.5× reference interval in >75% of cases)

Why do you get hypercholesterolemia with hypothyroidism

Increased concentration of HDLs

Why do you get hypertriglyceridemia with hypothyroidism

Increased LDL, VLDL, and hyperchylomicronemia

What can hypertriglyceridemia in hypothyroidism lead to

Atherosclerosis: a disease where fat, cholesterol, and calcium build up as sticky deposits called plaque inside your artery walls, which narrows the vessels and slows down oxygen-rich blood flow

What is is virtually diagnostic for hypothyroidism in dogs

Elevated cholesterol, in combination with clinical signs

What will you see on CBC with hyperthyroidism

Erythrocytosis and increased MCV

± Stress leukogram (leukocytosis, lymphopenia, eosinopenia)

Heinz bodies, ↑ Factor VIII (risk of thrombosis)

What will you see on chemistry with hyperthyroidism

↑ ALT/ALP (liver effects, bone metabolism)

↑ LDH, AST

↑ bilirubin

↓ cholesterol (↑ hepatic clearance), ↑ glucose (stress, intolerance), ↓ fructosamine (unreliable for DM), azotemia (33%), masked renal disease due to ↑ GFR (↑ P)

What will you see on renal/ua with hyperthyroidism

↓ USG (1.006–1.060, medullary washout, ADH inhibition)

± proteinuria

Some cats have UTI but subclinical

What is the most consistent chemistry finding in dogs with hypothyroidism?

Hyperlipidemia (increased triglycerides and cholesterol)

What are clinical signs of hypothyroidism

Weight gain

Lethargy/mental dullness

Dermatological: rat tail, seborrhea, back of rear legs, poor wound healing, non-pruritic, acanthosis nigricans

Heat seeking/cold intolerance

Bradycardia

Constipation

Muscle weakness/atrophy

Edema

What does T4 and T3 do in the body

Metabolism

O2 consumption

Positive ionotrope and chronotrope

What is the difference between T4 and T3

T4: bound, DIT/DIT (Diiodotyrosine x 2)

T3: biologically active, DIT/MIT (Diiodotyrosine and monoiodotyrosine)

What are steps in thyroid hormone synthesis and release

Iodide oxidation: thryoid peroxidase

Formation of iodothyronines in thyroglobulin: DIT/DIT= T4 or DIT/MIT= T3

Secretion: endocystosis of colloid

All steps stimulated by TSH

What is the prevalence of hypothyroidism

0.2% highly diagnosed

What can cause primary hypothyroidism

75% must be destroyed before clinical sings

Lymphocytic thryoiditis (50% cases, leakage of thyroglobulin, fibrosis and inflammation, immune mediated 42-59%)

Idiopathic thyroid atrophy (50% of cases, adipose tissue)

Neoplasia (destructive tumors)

Adenomatous hyperplasia (rare, intrathryoidal metabolic defect)

Iatrogenic (sx, I131, antithyroid drugs)

What do thyroid carcinomas do in dogs

Destructive!!! lead to hypothyroidism

Which animals usually get iatrogenic hypothyroidism

Cats due to sx, I131 or antithyroid drugs to tx hyperthryoidism

What can cause secondary hypothyroidism

RARE pituitary malformation/neoplasia (loose all TSH)

What happens in cretinism

Congenital hypothyroidism that is rare and is caused by iodine deficiency leading to thyroid dysgenesis or dyshormonogenesis