Other/pansystemic/repro/stats etc Flashcards

(19 cards)

1
Q

what are the two phases of the cell cycle and what is eac divided into ?

A

Interphase
- G1 preparation (cell growth, protein synthesis)
- G2 DNA replication
- G3 (some texts) condensation of genetic material

Mitosis
- prophase
- metaphase
- anaphase
- telophase

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2
Q

what is the role of p53

A
  • regulates the cell cycel
  • when DNA is samaged it arrests the cell cycle allowing for repair vs apoptosis

mutations of p53 are present in most cancers. These cells will continue dividing regardless of there being damage or not

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3
Q

What are common paraneoplastic syndromes?
key points

A

Hypercalcaemia
- 2/3 of dogs with cancer
- Most common tumours lymphoma (PTHrp), AGASACA (PTHrp), multiple myeloma with lytic lesions
- 1/3rd of cats with cancer
- Tx rehydration and diuresis, furosemide, biphosphanates, prednisone/treat the cause

Hypoglycaemia
- insulinoma is key

Hyperviscocity syndrome
- multiple myeloma and polycythemia vera
- Cx; ataxia, depression, seizures, bleeding, epistaxis, exercise intollerance and syncope
- Tx; plasmapharesis, treat underlyng cause
- - MM; melphalan + pred
- -Plycythemia vera; phlebotomy + hydroxyurea
- - CCL - chlorambucil and prednisone

Anemia
- several mechanisms from IMHA, bleeding, chronic disease etc
- erythrocytosis - can occur due to EPO- like tumour producers ( enal carcinoma, renal T cell lymphoma, Nasal fibrosarcoma, Diffuse bronchoalveolar carcinoma, polycythemia verra_

Thrombocytopaenia
- several causes

Neutrophilik leukocytosis

Myasthenia gravis -> lymphoma

Mypertrophic osteodystrophy -> PTrh

Ectopic ACTH secreting tumour -> primar ylung tumour

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4
Q

what are the three types of hypertension ?
Define?

A

Situational -> white coat syndrome vs technique taken, ie standing vs trying to get up etc

Secondary -> pathological increase in hypertension as a consequence of a disease process causing hypertension

Idiopathic -> AKA primary or essential. No identifuable underlying cause

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5
Q

what are the most common causes of secondary hypertension in dogs and cats?

A

Dog;
- Chronic kidney disease
- Acute kidney disease
- Hyperadrenocorticism
- Diabetes mellitus
- Obesity* - effects considered to be small
- Pheochromocytoma
- Primary hyperaldosteronism

Cat;
- Chronic kidney disease
- Diabetes mellitus
- Hyperthyroidism
- Primary hyperaldosteronism
- Hyperaldosteronism.

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6
Q

How do you diagnose primary hypertension ?

A

sustained hypertension in the presence of normal CBC, Chemistry, UA.

USG < 1.030 does not necessary indicate that underlying kidney disease is the cause due to the pressure natriuresis; however, if USG > 1.030, less likely that you are dealing with underlying renal cause

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7
Q

What are target organs for hypertension - define each and how do you work this up ?

A

Kidneys
- progression of CKD
- Proteinuric = more rapid progression of renal disease
- Clinical findings; progression of CREA, SDMA, decrease FGR. Persistent proteinuria and microalbuminuria
- Workup= Renal parameters, urinalysis, GFR measurement

Eyes
- retinopathy chondropathy - very common in cats
- Reported in BP as low as 168 but >180 increased risk
- Cx; exudative retinal detachment, other lesions (retinal vessel tortuosity, multifocal retinal oedema)

Brain
- encephalopathy/stroke
- White matter edema and vascular lesions can occur
- 25-47% of hypertensive cats will have neuro signs
- Cats can also get ischaemic myelopathy in the cervical spine resulting in ambulatory tetraplegia with intact nociception

Heart/blood vessesl
- HCM phenotype due to increased afterload
- Aortic aneurysm and rupture is rare in both species.

brain
heart and blood vessels

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8
Q

you have a young healthy puppy with mild hypertension. How do you treat?

A

High BP in young, apparently healthy animals should be considered to be situational hypertension and does ** not** require treatment.

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9
Q

How do you diagnose hypertension?

A

If end-organ target damage, single blood pressure measurement are enough

If no end-organ target damage > 2 occasions of hypertensive measurements are needed.

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10
Q

What are the hypertension threshold?

A

Hypertension – based on the risk of end-organ damage
- Normotensive SABP < 140 mmHg
Pre-hypertensive (Low TOD risk) 140 -159 mmHg
- Hypertensive (Moderate TOD risk) 160-179 mmHg
- Severely hypertensive (High TOD risk) > 180 mmHg

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11
Q

As per ACVIM consensus statement. How do you treat hypertension in dogs?

A

Should be initiated when patient at the hypertensive or severely hypertensive range with the goal of keeping blood pressure in the (normotensive, pre-hypertensive range)
- Patient in the pre-hypertensive category (monitor q 6 months)

Once diagnosis is confirmed;
- search for underlying causes and treat if possible
- RAAS inhibitors; indicated in CKD, idiopathic hypertension
-> ACEi First line
-> ARB
- Calcium channel blockers (amlodipine)
- > second line - motor kidney parameters
- Diet; avoid high dietary NaCl intake (help reduce RAAS activation

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12
Q

Why may calcium channel blockers precipitate kidney disease in hypertension ?

A

They prefferentially dialate the afferent renal arteriole, which will increase RBF potentially worsening kidney damage

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13
Q

How do ACEi, ARB and Calcium channel blockers differ from one another?

A

ACEi and ARB target RAAS.
- ACEi angiotensin I-> II conversion
- ARB angiotensin II receptor blocker

Calcium channel blocker
- dihydropyridine -> amlodipine, stop Ca entry into the cell -> vasodilation
- Non dihydropyrimidine -> not used in hypertension

One key difference is that ACEi and ARB preferentially DILATE the efferent renal artery reducing glomerular hydrostatic pressure. Calcium channel blockers vasodilate the afferent renal artery which can increase RBF potentially leading to renal damage

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14
Q

How do we treat hypertension in cats as per the ACVIM consensus statement?
- what are potential side effects of these?

A

First line
- Amlodipine; can cause gingival hyperplasia, peripheral edema
- Not associated with increased survival despite control of hypertension
- ARBs; Indications: cat with chronic kidney disease and proteinuria

ACEi
- not indicated as first line

Note; if hyperaldosteronism is the cause -> spironolactone + adrenalectomy
Side effects of spironolactone in cats inclde facial escortiction and dermatitis

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15
Q

How do you treat a hypertensive crisis?

A

Fenoldopamine; If presenting with acute end organ damage;
Anti-hypertensive that can be used in a hypertensive crisis. It is a dopamine1-agonist which can cause renal arterial vasodilation, natriuressi and ncrease GFR. Has a short T1/2 so often given as a CRI

Patient with severe hypertension but no signs of acute end organ damage can be treated with PO medication instead
- Amlodipine
- Hydralazine (direct vasodilation)

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16
Q

What is sensitivity and specificity ?

A

A highly sensitive test means it’s good at detecting the disease when it’s present, minimizing false negative results (where the test incorrectly indicates someone does not have the disease when they do).

Specificity:
A highly specific test means it’s good at correctly identifying those who do not have the disease, minimizing false positive results (where the test incorrectly indicates someone has the disease when they don’t
- i.e. it does not get confused by other diseases

17
Q

What is positive and negative predictive value?

A

Positive predictive value – the probability that a patient with an abnormal test actually has the disease

Negative predictive value – the probability that a patient with a negative test result actually does not have the disease

18
Q

what is the sensitivity ?
Specificity?
Positive predictive value ?

A

Sensitivity; 80/(80+10)= 88%
Specificity; 70/(70+5)=93%
Positive predictive value; 80/85=0.94

19
Q

How do you calculate;
False negative rate
prevalence
sensitivity
specificity
positive predictive value
negative predictive value

Use table bellow

A

False negative rate = 1 – sensitivity
Prevalence = A+C /A+D
Sensitivity = A/A+C
Specificity = D/B+D
Positive predictive value = A/A+B
Negative predictive value = D/ C+D