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VTS ECC > Misc > Flashcards

Misc Flashcards

1
Q

What recumbency should you record an ECG in?
How many leads should you use?

A

Right lateral
Minimum 6 can use 12

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2
Q

Aldosterone

A

Made be the adrenal cortex
Causes sodium and water retention
Causes potassium loss

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3
Q

How does hypothermia cause bradycardia?

A

Causes decreased cardiac depolarisation
Decreases HR
Decreases CO

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4
Q

What does RAAS stand for?
What are the steps?

A

Renin angiotensin aldosterone system
1. Drop in BP sensed
2. JG cells in the kidney produce Renin
3. Angiotensinogen released from the Liver
4. Angiotensin I created
5. Converted via ACE to angiotensin II
6. Angiotensin II causes vasoconstriction and promotes the release of Aldosterone and ADH

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5
Q

Cells in the Pancreas and what they produce

A

Alpha cells - Glucagon
Beta - Insulin
Delta - Somatostatin
F Cells - Pancreatic polypeptide

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6
Q

Main electrolyte abnormalities with DKA

A

Hypokalaemia
Hyponatraemia
Hypophosphataemia
Hypomagnaesaemia

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7
Q

Calculation of free water deficit

A

BW x 0.6 x (Measured Na/140)

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8
Q

Information about Magnesium

A

2nd most abundant cation
Intracellular, less than 1% found in serum
Difficult to measure as only the ionised is active
Can be supplemented if refractory hypokalaemia
0.25-1mEg/kg/24hrs iv

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9
Q

Drugs that cause/ worsen hyperkalaemia

A

Ace inhibitors (enalapril or benazepril Fortekor)
Angiotensin receptor blockers (losartan and telmisartan Semintra)
Heparin
Cyclosporin
Tacrolimus
NSAIDS
Trimethoprim
Non-specific beta blockers
Cardiac glycosides

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10
Q

Renal threshold for glucose

A

Dogs 200 mg/dL (11)
Cats 220 mg/dL (12)

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11
Q

Difference between PvCo2 and PaCo2

A

PvCo2 is 5-10mmHg higher

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12
Q

Receptors in the CRTZ

A

Nk1
Dopamine
Serotonin
Histamine
Muscarine
Enkephalin
Alpha-2 Adrenergic

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13
Q

What receptors does maropitant act on

A

Nk-1 in the CRTZ

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14
Q

Why do severely anaemic patients not become cyanotic?

A

To become cyanotic you must have a haemoglobin level of above 5 (HTC 15%)

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15
Q

What temperature should you start active cooling?

A

Above 105.8 (41)

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16
Q

Plasma osmolality equation and normal

A

(2xNa) + BUN/2.8 + Glu/18
Normal 300

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17
Q

What is glyconeogenesis?

A

When the liver converts glucose to glycogen for sugar storage

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18
Q

Difference between endocrine and exocrine

A

endocrine - hormones
exocrine - enzymes

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19
Q

Normal blood lactate?
Indication of survival

A

Less than 2-2.5
How quickly it reduces

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20
Q

When performing abdominocentesis on a GDV which side should if be performed on and why?

A

Left lateral, perform from the right, to avoid the spleen

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21
Q

ARDS diagnosis
Berlin criteria

A

Acute onset - less than 72hrs
Prescence of a primary dx process that causes enough inflammation to set up a reaction in the lungs
Evidence of pulmonary oedema without heart failure or fluid overload
Evidence of inefficient gas exchange (P/F ratio >300)

P/F ratio >100 severe
100-200 moderate
200-300 mild

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22
Q

6 Organs involved in the SOFA score and Parameters measured

A

Respiratory
Liver
Cardiovascular
Renal
Coagulation
CNS

P/F ratio
Platelet count
Total bilirubin
Crea
MAP BP
GCS

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23
Q

3/4 Stages of ARDS

A
  1. Exudative
    Type 1 pneumocystis are damaged- they are in charge of gas exchange, they cannot multiply
  2. Proliferative
    Type 2 pneumocytes multiply- secrete surfactant
  3. Fibrotic
  4. Recovery
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24
Q

Types of fluid found in the pleural space

Disease processes associated with them

A

Transudate
Clear, low cell count, low protein count
Associated with decreased oncotic pressure- hypoalbuminaemia

Modified transudate
Most common, higher cell count
Associated with increased hydrostatic pressure- Heart failure

Exudate
High cell count, bacteria, lymphocytes
Pyothorax, chylothorax

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25
Q

What is MDR-1

Implications of genetic predisposition and not having it

A

Multi-Drug resistant protein - 1

Removes foreign substances out of cells in the GI tract, kidney, liver. Cannot stop drugs crossing the blood brain barrier
drugs have a larger effect, animals more sensitive

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26
Q

Things that affect absorption of drugs administered PO

A

Stomach, gastric motility

Lack of small intestinal motility. Drug can be reabsorbed + build up to toxic doses

Food in the stomach

Gastric pH

Increased permeability of the GI tract-more absorption

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27
Q

What is pharmacokinetics?
What is ADME?

A

The study of how drugs pass through the body

Absorption
Distribution
Metabolisation
Excretion

28
Q

Drugs that activate the P450 system and increase metabolism

A

Phenobarbitone
St johns wort
Phenylbutazone

29
Q

Drugs that decrease the metabolism of other drugs

A

Erythromycin
Grapefruit juice
Omeprazole
Cimetidine
Chloramphenicol

30
Q

What causes the oxyhemoglobin curve to shift to the right?

A

decreased pH
Increased temperature

31
Q

What causes the oxyhemoglobin curve to shift to the left

A

Increased pH
Decreased temperature

32
Q

What causes the oxyhemoglobin curve to shift to the left

A
33
Q

Normal circulating blood volume

A

90ml/kg dogs
55ml/kg cats

34
Q

How much FFP does it take to increase albumin by 1g/L (10g/L UK)

A

45ml/kg

35
Q

Units for albumin and the difference?
Normal range

A

US g/Dl
Uk g/l
x10

3.2-4.1

36
Q

4 types of hypoxia

A

Hypoxic
Hypaemic
Histiotoxic
Metabolic

37
Q

5 causes of hypoxaemia

A

V/Q mismatch
Low partial pressure of inspired O2
Diffusion impairment
Anatomical shunting
Hypoventilation

38
Q

What is shock

A

A severe imbalance between oxygen supply and demand. Leading to inadequate cellular energy production, cellular death and multi-organ failure

39
Q

Units for creatinine and how to convert

A

x88
US mg/dL
UK mol/L

40
Q

Differences between abdominal fluid and peripheral blood that can show uroperitoneum

A

Potassium x1.4 more
Creatinine x2 more

41
Q

What vitamin helps with the absorption of calcuim

A

Vitamin D3
Cholecalciferol

42
Q

What are kupffer cells and were are they found?

A

Macrophages found in the liver
Remove bacteria from the blood

43
Q

Definition of sepsis

A

A life threatening organ dysfunction caused by a dis-regulated host response to infection

44
Q

Metabolic deficits seen with hepatic lipidosis

A

Glutathione
Taurine
Vitamin K
Vitamin B

45
Q

Definition of septic shock

A

A subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality
Inability to maintain BP abouve 65MAP despite adequate fluid resuscitation without vasopressors
Lactate will not go below 2

46
Q

Where is glucagon produced?
What does it do?

A

In the pancreas
Stimulates the liver to convert stored glycogen to glucose for energy

47
Q

Which vitamin is needed for the production of haemoglobin?
Where is it stored?

A

B12 Liver

48
Q

Drugs you wouldn’t give to patients with kidney problems

A

NSAIDS
Some diuretics
Some antibiotics
Tetracyclines and Sulphomimides
Corticosteroids

Decreased clearance, narrow safety margins

49
Q

Differences between abdominal fluids and peripheral blood that can show septic effusion

A

Glucose lower in effusion (20)
Lactate higher (2)

50
Q

Effects of metabolic acidosis on the body

A

Shifts oxyheam curve to the right
Decreases cardiac contractility
Decreased CO
Tachycardia
Decreased arrhythmia threshold
Catecholamine resistance
Peripheral arteriolar vasodilation
Venoconstrication of peripheral veins
Pulmonary arteries vasoconstrict
Insulin resistance
Hyperkalaemia (K swapped from cells with H)

51
Q

Risks associated with administration of sodium bicarbonate

Calculation for the amount needed

A

Paradoxical cerebral acidosis
Increased Co2 production
Hypercapnia
Increased sodium and osmole concentration
Circulatory system overload
Iatrogenic metabolic alkalosis
Changes to oxyhemoglobin curve
Hypocalcaemia
Hypokalaemia

mEg of bicarbonate needed = 0.3xBWxbase excess

52
Q

2 major stimuli for ADH release

A

Elevated plasma osmolality
Decreased effective circulating volume

53
Q

Effects of alkalosis on the body

A

Muscle spasms
Stuporous mentation
Hypocalcaemia
Hypokalaemia

54
Q

Difference between anions and cations and examples of both

A

cations are positively charged
K+
Na+
Mg+
Ca+

Cl-
HCO3-
P-

55
Q

How to convert glucose and the units?

A

UK mmol/l
US mg/dL
/18

56
Q

What is apheresis

A

When the blood is removed from the patient and separated into its components
One or more components id removed or processed and the blood is returned to the patient

Therapeutic plasma exchange

57
Q

What type or reaction is anaphylaxis?

A

IgE mediated hypersensitivity reaction

58
Q

Stages of hypovolemic shock and clinical signs associated

A

Compensatory
Vasoconstriction
Splenic contraction
Tachycardia
Rapid CRT
Injected mm’s

Early decompensatory
Tachycardia
Hypotension
Weak pulses
Pale mm’s
Prolonged CRT
Cool extremities
Increase in resp rate and effort
Decreased mentation

Late decompensatory
Bradycardia
Severe refractory hypotension
Pale/cyanotic mm’s
Undetectable CRT
Weak/absent pulses
Hypothermia
Decreased mentation
Prolonged and severe tissue hype-perfusion causes ATP deplation, anaerobic respiration and cellular death

59
Q

What is cardiac afterload

A

The force that the ventricles must overcome to open the semi-lunar valves

60
Q

What is cardia preload

A

The volume in the ventricles at the end of diastole

61
Q

Nasal oxygen dose

A

50-150 ml/kg/min

62
Q

A-a Gradient and normal limits

A

PAO2-PaO2

PAO2=
(FiO2x713)-(PaCo2/0.8)

Normal = 5-15

63
Q

How to calculate MAP

A

((Diastole x 2)+ Systole) / 3

64
Q

What is released during anaphylaxis

A

Histamine
Cytokines
Heparin
Tryptase
Prostaglandins
Platelet activating factor

65
Q

What receptors does histamine bind to?

What effects are seen due to this?

A

H1-H4

(GI, CV and resp systems)

Respiratory signs, smooth muscle contraction, bronchospasm, mucus secretion, oedema formation
Cardiogenic shock
Dysrythmias
Cardiac ischaemia
Gastric acid production
Puritis
Increased vascular permeability
Vasodilation

66
Q

Normal level of lactate

A

> 2.5

VTS ECC (1 decks)

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