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SAMS > SAMS Midterm > Flashcards

SAMS Midterm Flashcards

1
Q

What is systemic blood pressure a product of

A

Cardiac output and systemic vascular resistance

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2
Q

What regulates systemic blood pressure

A

SNS and RAAS

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3
Q

How does stress increase blood pressure

A

During times of stress, the SNS increases release of catecholamines which causes vasoconstriction of smooth muscle and increases blood pressure

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4
Q

Where is ace made (angiotension converting enzyme)

A

The lungs

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5
Q

What do ace inhibitors do to the raas system

A

Ace inhibitors block the angiotensin converting enzyme which ultimately decreases angiotensin 2

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6
Q

What happens when perfusion to the kidneys decreases (regarding the RAAS)

A

The kidney releases renin which converts angiotensinogen to angiotensin I

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7
Q

How does Angiotension 2 affect vessels and smooth muscle

A

Causes vasoconstriction which increases blood pressure

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8
Q

What in the raas system leads to production of aldosterone

A

Angiotensin 2 acts on the adrenal gland to increase production of aldosterone

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9
Q

What is the function of aldosterone

A

Stimulate resorption of sodium and water

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10
Q

What classifies systemic hypertension

A

Persistent systolic pressure > 160 mmhg

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11
Q

What should you be looking for if you have a patient with systemic hypertension

A

An underlying cause (80% of cases are due to underlying causes)

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12
Q

What should you check next if you find retinal hemorrhage and sudden blindness in a patient

A

Blood pressure - suspect hypertension

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13
Q

Which method of blood pressure measurement is most effective in small dogs and cats

A

Doppler

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14
Q

What blood pressure measurement is best for medium to large dogs

A

Oscillometric

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15
Q

How can you measure blood pressure directly

A

Arterial catheterization - usually under anesthesia

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16
Q

What are 2 indirect ways to measure blood pressure

A

Doppler and oscillometric

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17
Q

How do you determine what blood pressure cuff size you should use

A

Cuff width should be 30-40% circumference of where it is placed

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18
Q

Where can you place blood pressure cuffs (indirect)

A

Limbs or tail

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19
Q

Where on the limb do you place the blood pressure cuff on the limb? Tail?

A

On limb- under the metatarsal or carpal region
Tail - close to the bag

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20
Q

What are possible targets organs of damage that could be affected by systemic hypertension

A

Eyes, kidneys, brain, heart and vasculature

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21
Q

How can hypertension damage the kidneys (TOD)

A

Will see increased proteinuria or rapid progression of ckd

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22
Q

What is a pre hypertensive bp range

A

140 - 159 mm Hg

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23
Q

What is a normotensive bp range

A

<140 mm Hg

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24
Q

What is hypertensive pp range

A

160 - 179 mm hg

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25
Q

What is a severely hypertensive bp range

A

> 180 mmhg

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26
Q

What are the two most common causes of underlying hypertension in cats

A

Chronic kidney disease ( the most common) and hyperthyroidism

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27
Q

What medications can increase blood pressure

A

Corticosteroids, prion, erythropoietin agents

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28
Q

What are the 2 most common underlying causes of hypertension in dogs

A

Kidney disease (acute or chronic, where as cats are usually chronic) and hyperadrenocorticism (cushings)

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29
Q

When should you treat hypertension

A

Persistent bp over 160 mmhg and causative disease , severe hypertension (>180 mmhg) or evidence of Target organ damage with moderate to severe hypertension

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30
Q

What is the first line of treatment for cats with systemic hypertension

A

Amlodipine - calcium channel blocker (relaxes smooth muscle and cause vasodilation, decreasing bp)

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31
Q

When should you recheck blood pressure after treating systemic hypertension with amolodipine and why

A

7-10 days became that is when drug takes max effect

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32
Q

When is ambodipire used to treat hypertension in dogs

A

When severe >180 mmhg

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33
Q

How do Ace inhibitors treat systemic hypertension

A

Ace inhibitors block Ace which stops the production of angiotensin 2 (which causes vasoconstriction) and then decreases proteinuria ; vasodilates the efferent arteriole to decrease pressure in the glomerulus and help with the hypertension

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34
Q

What type of drugs are enalapril and benazepril

A

Ace inhibitors

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35
Q

What is a benefit of Ace inhibitors compared to amlodipine

A

Ace inhibitors have a more direct effect on the kidneys (can cause a potential drop in GFR and can reduce proteinuria)

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36
Q

What is a potential risk of using ace inhibitors

A

Can cause development of azotemia (increased bun and creatinine /ck) due to decreased glomerular filtration rate

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37
Q

What is the list line of treatment for systemic hypertension in dogs (with what exception)

A

Ace inhibitors except if severe hypertension >180-200 mmhg ( then use amlodipine (a calcium channel blocker) in combo with ace inhibitors)

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38
Q

Do Ace inhibitors work to control systemic hypertension

A

Barely - only reduce bp by 10 or so

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39
Q

If you find a dog with Addison’s like lab values (decreased sodium, increased potassium, increased cortisol), what question should you ask the owner

A

Is the patient on ace inhibitors

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40
Q

If Tod is present with severe hypertension, when do you check bp

A

Even 3 days (7-10 days if no Tod)

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41
Q

What goal bp are you truing to reach when feeling systemic hypertension

A

110 - 140 mmhg

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42
Q

With a bp of less than 120 mm hg and clinical signs of disease I what is indicated

A

Hypotension

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43
Q

What is spironolactone used for

A

Treat hypertension by acting as a aldosterone antagonist and diuretic - reduces sodium and water reabsorption

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44
Q

What treatment is used for pheochromocytomas (excess catecholamine production - adrenal tumors)

A

Alpha adrenergic antagonists because nothing else really works

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45
Q

What emergency drugs can be used to treat severe life threatening systemic hypertension and what is the risk

A

Direct arterial vase dilators ( hydralazine), risk for hypotension (profund quick vasodilation)

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46
Q

What is telamisartin

A

Angiotensin 2 receptor blocker - used for moderate hypertension in cats to reduce proteinuria ( can be used in dogs too); alternative to using ace inhibitors

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47
Q

What are two examples of alpha adrenergic antagonists

A

Phenoxybenzamine and prazosin

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48
Q

How does telmisartan work

A

Inhibits RAAS by blocking action of angiotensin 2 (blocks vasoconstriction and aldosterone production)

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49
Q

What is used to that severe life threatening hypertension

A

Direct arterial vasodilators (hydralazine and sodium nitroprusside)- only use in emergencies due to risk of profound hypotension; monitor with arterial line

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50
Q

Spirolectore is - sparing and useful to treat -

A

Potassium sparing and used to treat hyperaldosteronism

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51
Q

What are differentials for petechia

A

Def: Red or purple spots indicating hemorrhage under the skin
Diff: thrombocytopenia, endothelial dysfunction, thrpmbocytopathia

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52
Q

Loss than 50,000 platelets leads to concerns for

A

Spontaneous hemorrhage

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53
Q

Decrease albumins and increase globulins often indicate

A

Inflammation

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54
Q

What are 4 causes of thrombocytopenia

A

Decreased production, immune mediated destruction, consumption, sequestration

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55
Q

What tick transmitted disease can lead to pancytopenia (bone marrow disease)

A

Ehrlicia Canis - rickettsial disease

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56
Q

What on a blood smear can indicate Ehrlicia Canis (but does not rule it out if it is not there)

A

Morula in monocytes plus clinical findings

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57
Q

What is CME in regards to ehrlicia Canis? How and where is it transmitted

A

Canine monocytic erhlicosis - transmitted by the brown dog lick and found in warmer climates

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58
Q

What is the name of the brown dog tick

A

Rhipecophalus sanguireus

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59
Q

Describe the acute phase of E. Canis - when does it occur

A

Happens 8 - 20 days after inoculation - leads to fever, lethargy , peripheral edema , thrombocytopenia and thrombocytopathia , near signs, lymphadenopathy, hepatosplenomegaly (because the liver and spleen are big lymphoid organs)

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60
Q

When will the acute phase of E. Canis recover

A

May spontaneously recover after 2-4 weeks will eliminate infection or remain subclinically infected

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61
Q

Describe the chronic phase of E. Canis infections

A

Panculopenia due to bore marrow hypoplasia, marked lymphocytosis , bone marrow plasmacytosis

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62
Q

How do you diagnose E. Canis infection

A

Morulae visualized in monocytes or lymphocytes on blood smear - harder with chronic infections better with splenic or lymph node aspirates

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63
Q

Antibody testing indicates - but - not _

A

Indicates exposure but not active infection

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64
Q

What is the serological gold standard to diagnose E Canis

A

Indirect immune fluorescent antibody test (ifa) - IgG antibodies reliably indicate exposure L2 consecutive tests 7-14 days apart best to determine acute nation)

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65
Q

What suggests an acute and active infection of E. Canis

A

Four fold increase in ig G antibodies between 2 consecutive IFA tests

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66
Q

Whole blood PCR is more sensitive for _infections while serology is more sensitive for - infections

A

Whole blood pcr - acute infections (because DNA is still present)
Serology - chronic infections

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67
Q

What is the treatment for E-canis

A

Doxycycline -improvement after 24 - 48 hours

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68
Q

What breed is more sensitive to E. Canis infections and have a worse prognosis

A

German shepards

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69
Q

What is transmitted by the lone star tick and causes monocytic ehrlichiosis in humans

A

Ehrlicia Chaffeenis - rarely causes clinical signs in dogs but dogs can be a reservoir for infection to humans

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70
Q

What are differentials for joint effusion and lameness

A

Polyarthritis - either erosive or nonerosive (idiopathic versus septic)

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71
Q

What are differentials if a morula is found in a neutrophil ( specifically granulocytes) on a blood smear

A

Anaplasma phagocytophilium or erhlicia ewingii (granulocytes)

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72
Q

Both A. Phagocutophilium and E. Ewingii cause - and can be treated with - , how can you differentiate between the two

A

On cause polyarthritis and can be treated with doxycycline , differentiate with PCR or serology

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73
Q

What is transmitted by the lone Star tick and cause granulocytic erhlicolisis (replicates in neutrophils )

A

Ehrlicia ewingii

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74
Q

A. American is the

A

Lone star tick

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75
Q

Describe clinical signs of E. Ewingii

A

Acute infection 3-4 weeks after inoculation, causes polyarthritis, fever, lymphadenomegaly, etc and often a milder infection compared to E. Canis

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76
Q

What is transmitted by ixodes tick, is commonly seen in infections with Lyme disease and causes granolocytic anaplasmosis

A

Anasplasma phagocutophilium - morale seen in neutrophils that can’t be differentiated from E. Ewingii

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77
Q

What are clinical signs seen with A. Phagocutophilium infections

A

Often see no signs, will not cause chronic infections, can cause nonspecific signs like fever/ lymphadenomegaly and polyarthritis

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78
Q

What is transmitted by Dermacentor tick (American dog tick )

A

Rocky Mountain spotted fever - Rickettsia ricketsi

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79
Q

Describe what happens with RMSF and what you might see clinically

A

Replicates in endothelial cells in small vessels which causes vasculitis and then consumption of platelets and coagulation factors, then thrombocytopenia due to immune mediated platelet destruction which can lead to excessive henormage or thrombosis

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80
Q

Which organs are most affected with RMSF

A

Skin, brain, heart, kidneys

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81
Q

Describe the progression of RMSF

A

Progresses rapidly over 2-14 days

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82
Q

How do you diagnose and treat RMSF

A

Diagnose with serologic testing (ifa), treat with doxycycline, purebreds most affected ) may clear infection spontaneously

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83
Q

What protozoan infection is must spread by ingestion of A. Maculatum the gulf coast tick

A

American canine hepatozoonosis - caused by hepatozoon Americanum

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84
Q

What clinical signs do you see with hepatozoon Americanum

A

Severe muscle wasting, hypesthesia, stiff gait _ signs wax and wane with severity

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85
Q

What on CBC could indicate infection of H. American

A

Elevated leukocytes, increased alp, hypoglycemia

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86
Q

Where do signs occur with H. Americanum infection

A

Periostea bore proliferation along the proximal limb bones

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87
Q

How do you diagnose H. Americanum

A

Blood smear, skeletal muscle biopsy, whole blood pcr

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88
Q

How do you treat H. Americanum

A

TCP - TMS , clindamycin, pyrimethamine and then decoquinate to prevent clinical relapses (which are common)

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89
Q

Describe Babesia Canis

A

Large piroform shaped Protozoa existing in single or paired erythrocytes usually transmitted by the brown dog tick (R. Sanginueus)

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90
Q

The differentiate between Babesia Canis and Babesia gibsonii

A

Small Protozoa in single entrochtes (Babesia Gibson I)

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91
Q

What are clinical signs of uncomplicated Babesia

A

Thrombocytopenia and imha

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92
Q

_ Have a high prevalence of B. Gibsoni without clinical signs likely due to

A

Pitbuls, transmission by bite wounds

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93
Q

How do you diagnose Babesia infections

A

PCR

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94
Q

How do you treat Babesia infections

A

B. Canis - imidocarb
B, gibsonii - Azithromycin (a macrolide)

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95
Q

Define anemia

A

Reduced oxygen carrying capacity from insufficient hemoglobin and red blood cell mass in the vessels

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96
Q

What are 3 general causes of anemia

A

Loss, destruction Or hypoplasia (not making new RBCs)

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97
Q

Destruction and lack of production tend to cause more _ signs

A

Gradual signs and changes - ABCs last in blood for 7 weeks (loss is usually more of a rapid and severe change)

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98
Q

How do you confirm anemia

A

PCV and TS - CBC is a sample and cant tell you how much blood is actually in the patient

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99
Q

What cause of anemia can not be detected by or confirmedwith bloodwork

A

Rapid blood loss - because hct and PCV are percentages of RBC in blood and there will be minima changes immediately after blood loss

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100
Q

Can a dog still be anemic with a normal PCV and hct

A

Yes - if caused by rapid blood loss (takes a few hours)

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101
Q

If you give a shock patient fluids after blood loss , what will happen

A

PCV will decrease not because you are causing an cremia, but because you ave revealing it (will not affect the #of RBC but will affect the percentage - think dilute koolaid )

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102
Q

Describe the PCV and TS result of anemia due to bloodloss

A

Ow PCV And TS - all of it is leaving with the blood loss; initially high TS and normal pcv but we almost always miss this phase

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103
Q

Describe PCV and TS with anemia due to destruction , what might the plasma look like

A

Decreased pcv and normal or increased TS - plasma might be yellow due to RBC destruction

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104
Q

Describe PCV and TS with dehydration

A

Both likely increased (concentrated koolaid)

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105
Q

Describe PCV and TS with inflammation

A

PCV normal, globulins cause an increase in TS

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106
Q

Describe PCV and TS with anemia due to lack of production

A

Decreased POV, normal or increased TS (concentrated koolaid)

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107
Q

Describe CBC changes for blood loss anemia - what is important to note

A

High reticulocytes (bone morrow should be making more RBC to replace loss) - this will take 2-3 days so o if it is acute bloodloss it might not be increased (pre regenerative anemia)

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108
Q

Describe a regenerative anemia on CBC and why

A

Macrocyctic, hypochromic, polychomasia (means a diff sizes and shapes )- immature ABCs are bigger and lighter colored

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109
Q

Spherocytes on a CBC / blood smear usually indicate

A

IMHA - immune mediated anemia due to destruction

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110
Q

Describe the CBC of an anemia caused by destruction (like IMHA) - what is the exception

A

Strongly regenerative response (see other flashcard), informatory leukogram, spherocytes _ Will not be the case if the bone marrow is damaged

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111
Q

Describe the CBC of anemia due to lack of production

A

Pancutopenia ( if bone marrow damaged), non regenerative anemia (no reticulocytes , normochromic normocytic

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112
Q

What are differentials for chronic anemia

A

Parasites , ulcers, cancer

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113
Q

What are differentials for acute anemia

A

Trauma, coagulopathy , cancer

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114
Q

Hemolytic anemia is almost always - and can be - or -

A

Immune mediated usually (other causes are toxins, infections, etc) - can be intravascular or extravasalar

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115
Q

How can you differentiate between extavascular and intravascular hemolysis

A

Extravascular - icterus due to biliary excretion of bilirubin
Intravascular - renal excretion of free hemoglobin

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116
Q

What are differentials for hypoplastic anemia due to lack of production

A

Refractory anemias (anemia of chronic disease or inflammation, renal failure, Iron deficiency) or bore marrow disorders

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117
Q

Are spherocutes bigger than RBC

A

No - smaller

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118
Q

Nucleated RBC on blood smear indicates

A

Regeneration

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119
Q

What disorder looks a lot like an IMHA

A

Zinc toxicosis - causes oxidative injury (so a regenerative cremia with low POV and normal TS - destruction)

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120
Q

What age group usually sees IMHA

A

4 years or older

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121
Q

Describe signs of zinc toxicosis due to something like a penny

A

Young, vomiting, regenerative anemia, hyper bilirubinemia, informatory leukogram , mild spherocytodis

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122
Q

Agglutination on a blood smear indicates

A

IMHA

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123
Q

How do you treat IMHA

A

Immune suppression (predrisone) and antitrombosis (either anticoagulants or antipktelets) _but prednisone increases risk of thrombosis so need one of the antithombolics the whole time

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124
Q

Bruising, signs of shock and a low pcV and TS indicate what type of anemia

A

Loss

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125
Q

Prolonged pt and PTT increase worry of

A

Blood loss, spontaneous hemorrange and congulopathies

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126
Q

What can you give to a patient who needs clotting factors

A

Whole blood or fresh frozen plasma

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127
Q

Describe an iron deficiency anemia

A

Chemic external blood loss - starts as a Nama non regenerative anemia, then progresses to microcutic, hypochomic and no reticulocutes latter regerection happens then slows then stops)

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128
Q

Cushings disease is -

A

Hyperadrenocorticism - adrenal glands overproducing cortisol

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129
Q

What results do u expect in a normal dog given the low dose dexmethasone suppression test

A

At hour zero, cortisol levels should be over 1, at hours 4 and 8 it should be below 1 due to complete suppression

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130
Q

Describe the low dose Dexamethasone suppression test

A

Give dex IV, which has a negative feedback response and suppresses CRH from the hypothalamus ,which suppresses ACTH from the pituitary gland which should drop the cortisol

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131
Q

What will a LDDST look like if cushings (hac) is very likely

A

Cortisol at hours 4 and 8 are above the RR (1) and also above the hour zero multiplied by 0.5 (50% of that hour zero value) 1 indicates a lack of suppression

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132
Q

Differentiate between pituitary dependent and adrenal dependent cushings

A

PDH - increased ACTH production from the pituitary gland ( pituitary tumor)
Adrenal dependent - increased cortisol release from the adrenal gland (adrenal tumor)

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133
Q

Can a LDDST tell you which type of cushings the dog has

A

No-just tells you if cushings is likely

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134
Q

What are common signs of cushings in dogs

A

Pu/pd, increased appetite, non pruitic truncal aloepecia, distended abdomen

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135
Q

Describe pituitary dependent Cushings LDDST results

A

4 and 8 har cortisols are above the RR (1) and either one or both of the 4 and 8 hour cortisols ave less than the 50% of hour zero cortisol but still above the RR of 1

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136
Q

Can all pituitary dependent cushings be determined by the LDDST

A

No- only 60% follow the pattern, the other 40% will just look like lack of suppression and will need further testing

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137
Q

How to you medically manage pituitary dependent cushings - explain side effects

A

Trilostane - do not give compounded, give with food to maximize absorption , can cause mild lethargy or huporexia for several days

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138
Q

How can you assess if trilostane is working? What is the goal

A

ACTH stimulation test - start 4-6 hours after morning dose - goal is a post ACTH cortisol of 1.5.5.5 with control of clinical signs (without trilostane - results would be over 22)

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139
Q

Describe the ACTH stimulation test

A

Give ACTH which shard cause the adrenal gland to increase cortisol

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140
Q

When do you first check trilostane response? Should aw increase the dose if it is not working

A

Check after diagnosis at 10-14 days to make sure cortisol is not too low , do not increase the dose became it en take a month to see full effects of the starting dose

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141
Q

What is the risk of uncontrolled cushings

A

Puts dog in a hypercoagulable state so the risk of thromboemboli increases

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142
Q

Will trilostane make a difference in the tumor on the pituitary when treating for PDH cushings

A

No-just helps treat the long term effects

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143
Q

What is the goal of trilostane treatment and how does that apply to dosing

A

Control clinical signs - don’t adjust dose it signs resolved and cortisol is 1.5 or above

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144
Q

What response are you looking for on an ACTH stimulation test

A

Exaggerated response (above 22) after 1 hour

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145
Q

Can you differentiate between the types of cushings with an ACTH stimulation test

A

No

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146
Q

How can you differentiate between types of cushings

A

Endogenous ACTH or abdominal ultrasound

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147
Q

What are the treatment options for adrenal dependent cushings

A

Trilostane to manage clinical signs or adrenalectomy

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148
Q

What result would you expect on endogenous ACTH if adrenal dependent cushings

A

If the adrenal tumor is making a bunch of cortisol, it feedback and tells the pituitary to stop releasing ACTH (so ACTH should be below RR

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149
Q

What would you see on abdominal ultrasound with pituitary dependent cushings

A

Bilaterally symmetrical enlargement of the adrenal glands because the problem is in the pituitary making too much ACTH

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150
Q

What would you see on abdominal ultrasound with adrenal dependent cushings

A

A mass in the affected adrenal gland and a normal or small contralateral gland

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151
Q

If you have a dog with increased liver enzymes and a LDDST resembling lack of suppression but is showing no clinical signs of cushings 1 do you treat

A

No - LDDST has low specificity so potential for false positives

152
Q

Can you have hypercalcemia with Cushings

A

No

153
Q

If there are no signs of cushings, don’t

A

Don’t test for cushings

154
Q

What are differentials for multifocal bleeding

A

Trauma or coagulopathy/ primary hemostatic disorder

155
Q

What are differentials for prolonged pt and ptt indicating a congulopathy

A

Anticoagulant rodenticide most likely it values are very high, liver failure and DIC don’t usually cause a super high increase (usually mild)

156
Q

Will giving packed RBC replace clotting factors

A

No - need whole blood or fresh frozen plasma

157
Q

Pt prolongs due to a loss of - while PTT prolongs due to loss of -

A

Pt - loss of factor 7
PTT - loss of factors 2,9,10

158
Q

When is whole blood good to give

A

Nupovolemic patient, coagulopathy (except platelet function probably won’t be sustained)

159
Q

When are packed red blood cells good to give

A

Normovolemic, anemic patients

160
Q

When is frozen plasma best to use

A

All coagulopathies , anticoagulant rodenticides, hypoproteinemia

161
Q

How long do you commonly give vitamin K

A

28 days - then recheck pt and ptt

162
Q

What are differentials for petechiation

A

Thrombocytopenia , thrombocytopathia, endothelial dysfunction

163
Q

Where does spontaneous hemorrhage usually occur and at what platelet number

A

Skin and git usually - 30,000 to 50,000 platelets concern for spontaneous hemorrhage

164
Q

What are general causes of thrombocytopenia

A

Destruction , decreased production, consumption, sequestration

165
Q

, Very low platelets (10 - 15,000) indicates

A

Primary immune mediated thrombocytopenia

166
Q

Why might you see splenomegaly in a case of coagulopathy

A

Sequestration in the spleen causing a thrombocytopenia

167
Q

What antigen in dogs is know for causing transfusion reactions

A

DEA - blood type testing

168
Q

What is best to replenish all the lost components of blood (proteins, platelets, clotting factors)

A

Whole blood - if not available, can combine packed RBC and fresh frozen plasma

169
Q

How do now treat primary immune mediated thrombocytopenia

A

Immunosuppressive dose of steroids

170
Q

What are reasons why the HCT can progressively drop but TS stay the same

A

Neoplasia causing proteins to be high or dehudation + lasix

171
Q

With acute hemorrhage diarrhea syndrome (AHDS/HGE) , when does diaries usually resolve

A

Within 5-7 days

172
Q

Differentiate between vomiting and regurgitation

A

Vomiting - abdominal contractions , might contain bile, nasuea or salivation
Regurgitation - passive, esophageal or thoracic disease

173
Q

A vomit that has a coffee ground appearance likely indicates

A

Partially digested blood, maybe from ulcers

174
Q

When is bilious vomiting syndrome most likely to occur

A

In the morning on an empty stomach

175
Q

A thyroid slip is most common in - and increases the concern for

A

Older cats - concerned for hyper thyroidisn

176
Q

What are differentials for primary GI disease leading to chronic vomiting

A

IBD, neoplasia, parasitism, idopathic gastritis, chronic gastric foreign body

177
Q

What are extra GI / systemic differentials for chronic vomiting

A

Hyperthyroidism, chronic pancreatitis hepatobilary disease , CKD, hypercalcemia

178
Q

What are common signs of hyperthyroidism

A

Left thyroid slip with good appetite and weight loss - does not have to have a thyroid slip

179
Q

Why could hypercalcemia cause chronic vomiting

A

Because it causes dismotility of the git

180
Q

What are differentials for weight loss with a normal appetite

A

Enteropathy (IBD, neoplasia), metabolic (hyperthyroidism or diabetes), exocrine pancreatic insufficiency (often have diarrhea as well)

181
Q

Can parasites cause chronic vomiting

A

Yes - also can cause weight loss with a good appetite

182
Q

What can you look at to assess liver function

A

Glucose, bun, billirubin, cholesterol

183
Q

What could cause a low albumin and a low globulin

A

PLE or bleeding/hemorrhage (a PLN would have low albumin but normal to increased globulins)

184
Q

Will you always see malena with GI bleeding

A

No - only 50% so do a fecal blood test

185
Q

When would you do a hypoallergenic diet trial? How do you do it

A

Only in stable patients, if suspecting food responsive IBD - put on a strict hydrolyzed or novel protein diet for 3 weeks

186
Q

What is the risk of albumin continually dropping in a PLE

A

Life twittering effusion can develop - need close monitoring

187
Q

What is the benefit of ultrasound over rads in cases of PLE

A

Better evaluation of soft tissue and mucosal lining of stomach, git

188
Q

Differentiate between surgical and endoscopic git biopsies

A

Surgical - full thickness success to al portions of the si
Endoscopic - includes mucosa and submucosa, access to only the stomach, duodenum and ileum

189
Q

How do you treat inflammatory bowel disease

A

Prednisolone (immunosuppressive steroids) - taper once albumin is controlled and signs go away (taper by 25 % every 2-3 weeks to lowest effective dose)

190
Q

What are side effects of prednisolore

A

Diabetes (monitor glucose - reversible if noticed early ), skin fragility, weight gain , polyphagia, pu/pd / increased risk of infection

191
Q

What is an option other than prednisolone in cats

A

Bodesonide - locally acting corticosteroid

192
Q

What are 2 antiemetic options for supportive care of chronic vomiting

A

Cerenia (maropitant) , ondansetron - an combine both if severe refractory vomiting occurs

193
Q

How could you differentiate between IBD and small cell GI lymphoma

A

PCR - treat the same but add chlorambucil for small cell lymphoma

194
Q

What are chronic vomiting differentials specific to dogs

A

Dietary indiscretion, bilious vomiting syndrome, pyloric hypertrophy, hypoadrenocorticism

195
Q

Describe small bowel diarrhea

A

Large volume of feces , normal or increased frequency, weight loss, melena, maybe vomiting

196
Q

Describe large bowel diarinea

A

Small volume, increased frequency, frank blood (hematochezia), teresmus /straining, pain or urgency to defecate

197
Q

What are differentials for chronic small bowel diarrhea

A

Primary GI (especially if chronic) - lymphangiectasia ,IBD, parasites, neoplasia, dietary indiscretion
Systemic - Addison, exocrine pancreatic insufficiency, hepatobiliary disease, chronic renal failure

198
Q

Differentiate between food allergies and food intolerance

A

Allergies - immune system involved , reacting against food proteins
Intolerance - trouble digesting, immune system not involved

199
Q

Which breed often gets lymphangiectasia ? Describe it

A

Dilation of superficial lymphatics (which help about fat from diet) until they burst open - fluid in the lacteals is instating which causes information and protein loss - yorkies poster child

200
Q

What would you expect to see on Chem if muscle washing

A

Low creatine because it is a by product of muscle metabolism

201
Q

How can you rule out hypoadrenocorticism (addisons disease)

A

Basal cortisol - rule out if 2 or more, if less than 2 need todo a full acth stimulant test

202
Q

How do you rule out exocrine pancreatic insufficiency

A

TLI - takes a few day; EPI usual causes an increase in appetite due to decreased absorption

203
Q

How can you rule out or differentiate between lymphangiectasia and IBD

A

Endoscopy or diet trial using low fat diet (because hydolyzed diets have a lot of fat in them and the lactase are not absorbing fats with lymphangiectasia)

204
Q

Differentiate between primary and secondary intestinal lymphangiectasia and treatment

A

Primary - breed predisposition (Yorkies), treat with low fat diet
Secondary - due to blockage of lymphatics because of neoplasia or inflammation (ibd, parasites, food allergies ) - treat by focusing on underlying cause and putting on a low fat diet or hypoallergenic diet

205
Q

What ave consequences of PLE

A

Thromboembolic disease ( hypercoagulae state), vitamin deficiencies und malnutrition , poor encotic pressure leading to effusion, edema, etc

206
Q

How do you rule out histoplasmosis

A

Urine antigen test

207
Q

What are differentials for large bowel diarrhea

A

Histocutic ulcerative colitis (boxer colitis- steroids can make this worse) , IBD, infectious (whipworms in colon), IBS- neoplasia

208
Q

What are the 3 types of IBD

A

Food responsive, antibiotic responsive,steroid responsive

209
Q

Describe the physiology of bilirubin

A

Old/senescent RBCs are stripped for parts, hemoglobin is released and converted to iron and biliverdin by macrophages which then reduce the biliverdin into unconjugated bilirubin, which is then conjugated by the liver to form soluble bilinbin that can now be excreted into the duodenum into bile

210
Q

Extravascular hemolysis an lead to an increase in -

A

Unanjugated bilirubin (hasn’t been conjugated by the liver yet)

211
Q

Describe prehepatic hyperbilirubinemia

A

Before the liver, body breaking down too many RBC (hemolysis) and overwhelming the system

212
Q

Describe hepatic hyperbilirubinemia

A

Breaking down normal amount of RBC but liver is not processing it as well, not being conjugated or excreted into bile

213
Q

Describe post hepatic hyperbilinbiremia

A

Problem after conjugation with getting out of the body, some obstruction between the liver and rectum

214
Q

What are differentials for prehepatic hyperbilinbiremia

A

Hemolysis, anemia, immune mediated (imha), toxin (zinc - penny), post transfusion (lots of old RBC)

215
Q

What are differentials for hepatic hyperbilirubinemia (functional problem)

A

Liver failure - toxins, hepatitis/infectious, cirrhosis (scar tissue), portosystemic shunts (end stage), microvascular dysplasia, secondary injury (hepatic lipidosis), congenital deficiencies ; prognosis really pour

216
Q

What are differentials for post hepatic hyper bilirubinemia

A

Billiary obstruction - gall bladder mucocele , cholethiasis (gallstones) , pancreatitis, tumors

217
Q

What do orange gums make you suspicious of

A

Some RBC plus icterus of hyperbilinbiremia - hepatic and post hepatic causes high an list

218
Q

Yellow/ icteric gums make you suscpicious of

A

Hemolysis - prehepatic hyperbilirubinemia

219
Q

How can you differentiate between causes of hyperbilinbiremia

A

PCV ICT to check for anemia, chem to check for liver leakage enzymes, ultrasound to check for mucocele

220
Q

It you have huperbilirobinemia and see diction of the common bile duct, what do you suspect

A

Suspect post hepatic

221
Q

How long before hyperbilinbirenia resolves

A

Slow - likes to sit in fit tissue so can still be icteric long after resolving the problem

222
Q

How much hyper bilinbirenia is needed to see icterus

A

3mg/dl

223
Q

What is the main function of the exocrine pancreas

A

Digestion and to package digestive ensures in a way to safely get to git without digesting the wrong thing

224
Q

What is pancreatitis

A

Information of pancreas - information causes leakage of digestive enzymes packaged by the exocrine pancreas that leads to digestion of local tissues, pain and inflammation

225
Q

What are signs of pancreatitis

A

Vomiting, diarrhea, abdominal pain (unlikely pancreatitis if not painful) , anorexia, dehydration, lethargy

226
Q

Is it super important to confirm suspected diagnosis of pancreatitis

A

No - treatment is most supportive care of symptoms

227
Q

What is the limitation with using biopsy to diagnose pancreatitis

A

Invasive and may not yet the affected part of pancreas (whole thing not always affected)

228
Q

What could a PLI help you diagnose

A

Pancreatitis (where as TLI diagnosis epi) - very good screening test

229
Q

How is a PLI (pancreatic lipase immunoreactivity) snaptest helpful in diagnosing pancreatitis

A

If negative, pancreatitis is unlikely, if positive could be but could also be other things

230
Q

If you get a positive PLI can you diagnose the dog with pancreatitis

A

No - keep diagnostics

231
Q

Do signs of pancreatitis wax and wane? Can pancreatitis be non painful

A

No and not usually no

232
Q

What is the treatment for pancreatic

A

Supportive are while body heals itself

233
Q

What is really important when treating pancreatitis

A

Managing pain

234
Q

The gut heals faster with -

A

Food - place NG tube when stable

235
Q

What is the most common endocrinopathy of cats

A

Hyperthyroidism - occurs in 15% of cats over 10 years old

236
Q

What is hyperthyroidism

A

Excess production of T4 and T3 (which suppresses TSH)- due to thyroid adenomas, adenomatous hyperplasia or rarely carcinoma

237
Q

What are the goals of hyper thyroid treatment

A

Achieve euthyroidism and avoid worsening kidney function bu making more hyper or hypothyroid

238
Q

What are the goals of hyper thyroid treatment

A

Achieve euthyroidism and avoid worsening kidney function bu making more hyper or hypothyroid

239
Q

How does hyperthyroidism affect kidneys

A

Hyper thyroid increases GFR which decreases creatinine - when you treat hyperthyroid you often unmask CKD in cats so warn owners

240
Q

What will always go dan when treating hyperthyroid in cats? What will go up when treating CKD

A

GFR will always go down, CK will go up when treating CKD

241
Q

How can you medically manage hyperthyroid in cats

A

Methimazole - cheap, effective long term, reversible, oral or transdermal application, tumors will still progress to carcinomas and methinazole resistance can occur

242
Q

What are side effects of methimazole

A

GI signs, hepatotoxicity, facial pruritis - usually seen in first few months

243
Q

How do you monitor metimazole

A

CBC / Chem and T4 in 2-4 weeks

244
Q

Describe surgical thyroidectomy for treatment of hyperthyroidism

A

Risk of hypothyroid and hypoparathyroid, recurrence ever when done bilaterally

245
Q

What is the treatment of choice for hyperthyroidism ? Describe it

A

Radioiodire - 95% efficacy with one treatment, destroys abnormal thyroid tissue - need 2 week at home isolation

246
Q

When are methimazole trials done before radioiodine treatment in hyperthyroid cats

A

In cats who are azotemic at diagnosis to monitor CK values

247
Q

Describe nutrition therapy for hyper thyroid cats

A

Low iodine diet, must be the only thing the cat eats - goal is to lower the thyroid hormone levels

248
Q

What are the benefits of feeding low iodine diets to hyperthyroid cats

A

Normalize T4, signs improve in 4 weeks , CK decreases

249
Q

When is it best to use nutrition therapy to treat hyperthyroid in cats? When is it hard

A

Best - cat can’t tolerate methinazole, concurrent disease or renal insufficiency
Hard - indoor/outdoor cats, multi households

250
Q

What is the most common case of hypothyroid

A

Iatrogenic when treating hyperthyroidism

251
Q

How often does hypothyroid occur when treating hyperthyroid

A

75% of cases treated with radioiodine (transient and most resolved by 6 months), 10% permanent, if methimazole induced it is reversible by lowering the dose

252
Q

Why is hypothyroid caused by treating hyperthyroid bad

A

More likely to be azotemic, decreased GFR, decreased survival - goal is euthyroid!

253
Q

What are clinical signs of hypothyroid

A

Weight gain, decreased appetite (opposite of hyperthyroid), pu/pd

254
Q

Which is a more accurate test for hypothyroid

A

Free T4 _ total T4 made more inaccurate by non thyroidal illness (like in cats with CKD have low T4)

255
Q

What indicates subclinical hypothyroidism

A

Elevated TSH with normal T4

256
Q

What is the most sensitive test for hypothyroidism

A

TSH

257
Q

When do you monitor post treatment of hyperthyroid

A

1 month - check for resolution of hyperthyroid
3 months - detect hypothyroid
6 mantas - determine renal function

258
Q

When do you treat hypothyroidism and how

A

Permanent it present at 6 month check - treat if new or worsening azotemia; treat with levothyroxine to increase GFR and improve kidney anchor

259
Q
  • Thyroid is most common in dogs 1 - thyroid is most common in cats
A

Hypothyroid - dogs, hyper thyroid - cats

260
Q

Describe total T4 as a diagnostic test

A

Very sensitive for diagnosing hypothyroid but not specific (false positives are common)

261
Q

What is the best thyroid function test available

A

Free T4 - highly sensitive and specific

262
Q

Testing TSH is used for

A

Diagnosing hypothyroid early - insensitive (only elevated in 60-75 % of hypothyroid) very specific

263
Q

What thyroid hormone values absolutely confirm hypothyroid

A

Low TT4 and free T4, high TSH

264
Q

TSH is produced by the - and inhibited by _ produced by the thyroid

A

TSH produced by the military and inhibited by thyroid hormones T4 and T3

265
Q

What are common signs of cushings

A

Pu/pd, weight gain, pot belly, polyphagia

266
Q

Will a hypothyroid dog have pu/pd

A

No never

267
Q

What are clinical signs of hypothyroid

A

Overweight, lethargic, exercise intolerant, non pitting edema causing a sad face, double chin look

268
Q

What are clinical signs of hyperthyroid

A

Thin, tachycardia, too much energy, trembling

269
Q

Why could a hypothyroid dog have an elevated TT4

A

Autoantibodies to T4 affecting it - less comments that the dog is actually hyperthyroid (if it was probably due to a malignant tumor - where as cats have benign tumors)

270
Q

Why could a hypothyroid dog have an elevated TT4

A

Autoantibodies to T4 affecting it - less comments that the dog is actually hyperthyroid (if it was probably due to a malignant tumor - where as cats have benign tumors)

271
Q

What kind of drugs can lower T4 making it look like hypothyroid

A

Phenobarbital, sulfonamides, glucocorticoids, NSAIDs

272
Q

What breed may have lowered T4

A

Sighthounds / greyhounds

273
Q

How do you treat hypothyroidism? How should you monitor

A

Levothyroxine - recheck signs 8 weeks later, 4 cars after giving the pill the T4 should be in the high normal range

274
Q

What value other than TSH is commonly high with hypothyroid dogs

A

Cholesterol

275
Q

Can you use free t4 alone to diagnose hyperthyroid in cats

A

No - non thyroidal illness can falsely increase it

276
Q

If TSH is normal, the cat is likely not

A

Not hyper thyroid

277
Q

What liver enzymes represent hepatocellular injury

A

Alt and AST

278
Q

What liver enzymes represent cholestasis /enzyme induction

A

Alp and GGT

279
Q

What liver enzymes indicate impaired liver function

A

Bilirubin, albumin, glucose, bun, cholesterol

280
Q

Describe alt and reasons it would be increased

A

Indicates hepatocellular damage or necrosis, has a short half life so it goes up then down quickly if persistently increased it indicates continued hepatocyte injury

281
Q

Define cholestasis

A

Decreased bile flow

282
Q

The alp value is a combination of

A

Liver, bone and corticosteroid isoenzymes

283
Q

Increased alp on be induced by what drug

A

Phenobarbital

284
Q

What disease in cats can cause increased alp and GGT

A

Hepatic lipidosis

285
Q

What can cause an increase in bilirubin

A

Hemolysis, bile tract disease and liver dysfunction

286
Q

What could cause albumin to be low

A

Low albumin indicates severe liver dysfunction as long as git and kidney loss are ruled out

287
Q

When does glucose decrease with liver injury

A

Decreased when over 75 % of liver function is lost

288
Q

What could cause bun to decrease

A

Decreased from PSS or chronic liver disease

289
Q

What to prolonged clothing times indicate

A

Significant hepatic disease or factor consumption

290
Q

What is the most sensitive liver function test

A

Bile acids - use to screen for loss of hepatic function or for PSS

291
Q

When are bile acids contraindicated

A

If hyperbilinbiremia or jaundice

292
Q

What is the most common cause of abnormal liver enzymes

A

Secondary to non hepatic disease (drugs, endocrine disease, dental disease, neoplasia, etc)

293
Q

When shard you investigate abnormal liver enzymes further

A

If alt is greater than twice Normal over several months, non hepatic causes ruled out or unexplained resistant elevation lasting 6-8 weeks

294
Q

What is the main stay of immunosuppressive therapies

A

Glucocorticoids - prednisolone and dexmethasone

295
Q

What are side effects of glucocorticoids

A

Pu/pd, panting, polyphagia , muscle atrophy, weakness - can induce inorganic cushings or amicably increase liver enzymes (alp)

296
Q

What are contraindications of steroids

A

Diabetes mellitus, infection, hyperadenocaticism, NSAID therapy

297
Q

What is the second line therapy for IMHO, IMTP, etc

A

azothioprine - glucocorticoid sparing effects, taper after prednisone!

298
Q

What is diabetes mellitus

A

A problem with insulin - either a lack of production or lack of response, characterized by hyper glycemia

299
Q

What is the problem with not having insulin

A

We need insulin to move glucose into cells (or the cells will starve) - the brain can still get glucose but the liver is very dependent on insulin for getting glucose

300
Q

Besides glucose, what else does insulin bring into the cells

A

Potassium and phosphorous

301
Q

When you give insulin, what will increase in the cell

A

Potassium, glucose, phosphorous

302
Q

Differentiate between type 1 and type 2 diabetes

A

Type 1 - lack of insulin production by Beta cells
Type 2 - resistance to the effects of insulin

303
Q

Describe the body’s response to various glucose states

A

It blood sugar is high - insulin released by pancreas to get glucose into cells
If blood sugar is low - pancreas shuts off insulin and turns on glucagon which cause, release of glucose from liver

304
Q

If insulin - then glucagon will -

A

If insulin increases, glucagon will decrease and vice versa

305
Q

What is plan B when there is no insulin

A

Fatty acids get converted to ketones - not as efficient Evers sure, less ATP, the liver cant use ketones but the brain can

306
Q

Are ketones always bad

A

No- sometimes can be good

307
Q

What are the 3 ketones (which are acids)

A

Acetone, acetoacetate, betahydoxy butyrate

308
Q

What is enough to diagnose keto acidosis

A

Diabetes melliits and acidosis with no other cause

309
Q

Why does keto acidosis occur with DM

A

Because body keeps making ketones (which are acidic ) to feed the cells that aren’t getting glucose - either are to poorly managed or unrecognized DM or a comorbidity develops with DM

310
Q

How do you treat DM? How do you treat dka?

A

Give insulin ! Reverse the ketoacidosis by feeding the cells

311
Q

Differentiate between types of insulin

A

Regular - short acting, similar to type made by pancreas, used in emergency diabetic crisis
Intermediate or long acting - used for managing DM, usually dosed twice a day, can also manage DKA

312
Q

Why is insulin intentionally short acting

A

Because once glucose changes it helps to be able to respond quickly

313
Q

What’s the difference in goals when treating DM and DKA

A

Dm-give insulin to decrease glucose
DKA give insulin to reverse the ketoacidosis and get rid of ketones (bring to DM)
Both - reverse starvation

314
Q

What are the components of total body water (70%)

A

Extracellular - interstitial or intravascular
Intracellular ( 66%)

315
Q

Describe the Sodium and potassium levels inside the cell, outside the cell?

A

Inside cell - high potassium, low sodium
Outside cell - high sodium, low potassium

316
Q

Describe the sodium and potassium in replacement and maintenance fluid

A

Replacement - high sodium low potassium
Maintenance - low sodium high potassium

317
Q

What’s the difference between a balanced and unbalanced

A

Balanced - similar to Extracellular fluid
Unbalanced - too much chloride compared to ecf

318
Q

Fluid tonicity indicates

A

How salty fluid is

319
Q

When is rehydration typically performed

A

Corrected over 12-24 hours - faster if renal injury or azotemia because you want to prevent further damage , slower if cardio disease

320
Q

Would you give a fluid bolus for dehydration

A

No - dehydration occurs too an correct slowly, only give bonus to hypovolemic patients or shock patients

321
Q

What is maintenance fluid rate

A

30 - 60 mL / day, neonates 80 - 120 ml/day

322
Q

What are potential complications of fluid therapy

A

Electrolyte imbalances , edema or pitting edema, iatrogenic CHF, phlebitis

323
Q

What is the last sign affected by giving fluids

A

Lungs - the filtering organs affected first (kidneys, liver

324
Q

What are the possible signs of fluid overload

A

Naseua , loss of appetite, regurgitation, hard swallowing, extended neck

325
Q

When should you discontinue IV fluids

A

When patient eating and drinking

326
Q

A high UPC ( urine protein to creatinine ratio) indicates

A

Glomerular disease

327
Q

A low UPC indicates

A

Tubular disease

328
Q

What are common presentations of a uremic crisis

A

Know history of CKD exacerbated by a complication or a secondary acute kidney injury or could not have a history of CKD and can look like acute kidney injury

329
Q

Differentiate between AKI and CKD

A
  • Both have apparent acute onset
  • anemia more likely in CKD
  • azotenia likely in both but patient feels much worse if due to AKI (no adjustment time)
  • history of muscle washing and long standing polydipsia
  • AKI leads to larger kidneys due to inflammation / ckd leads to small kidneys due to chronic infarcts
330
Q

What are common findings of CKD with acute kidney injury or exacerbation for other reasons

A

Dehydration, anorexia, vomiting, weakness, lethargy

331
Q

What are complications of CKD

A

Hypertension (then concurrent retinal damage ), secondary UTI

332
Q

How do you treat CKD with acute exacerbation

A

Correct dehydration (otherwise kidney damage increases), treat symptoms and correct any comorbidities

333
Q

Describe diuresis in terms of CKD and treatment

A

Kidneys filter more than normal fluid (polyuria) - good in cases of fluid overload, bad in cases of CKD - forced diuresis is when we give fluids and diuretics

334
Q

How do fluids treat CKD

A

They don’t! They treat dehydration and hypovolemia - fluid overload in CKD patients can actually be really bad

335
Q

Dehydrated parents with CKD should

A

Have their dehydration corrected aggressively then stopped quickly once fixed (in 8 - 12 hours)

336
Q

What is the only kind of azotemia that is corrected with find therapy

A

Prerenal

337
Q

Rehydration should be done using - and maintenance should be done using -

A

Rehydration - balanced electrolyte solution like LRS (lower in chloride and better for the kidneys)
Maintenance - low sodium find like half saline, discontinue gradually

338
Q

What are two at home treatment options for CKD patients if voluntary water intake is insufficient

A

Subcutaneous fluids or feeding tube placement (that is not used for feeding)

339
Q

What is a can of subQ fluids in a CKD patient

A

High in salt - makes kidneys have to work harder

340
Q

What is part of the laver urinary tract

A

Bladder, urethra, prostate

341
Q

What are recurrent LUT signs

A

Hematuria, strangeruria (pain on urination), pollikuria (urinating frequent small amounts )

342
Q

What meds are good for treating UTIs

A

Penicillins - tetracyclines don’t reach high concentrations in urine

343
Q

Differentiate between complicated and uncomplicated UTIs

A

Complicated - recurrence more than 3 times in a year, comorbidity or anatomic abnormality present I intact male dogs or cats often
Unemplicated - sporadic, otherwise healthy animal

344
Q

What do you use to treat complicated UTIs caused by prostatitis

A

Fluroquinolones like enrofloxacin

345
Q

What ave indications for a bone marrow aspirate

A

Unexplained thrombocytopenia or non regen anemia, staging of neoplasia, investigation of atypical cells, checking iron stores

346
Q

What are 3 possible sites for a bone marrow aspirate

A

Iliac crest of the pelvis, trochanteric fossa of the femur, greater tubercle of humerus

347
Q

Why do you put EDTA through the bone marrow sampling needle

A

To prevent clotting of blood

348
Q

What are indications of a thoracocentesis

A

Collect pleural effusion for cytology or relieve clinical signs of dyspnea caused by pleural effusion or pneumothorax

349
Q

What are contraindications for thoracocentesis

A

Coagulopathies unless a hemothorax caused by a coagulopathu

350
Q

Where do you insert the needle for a thoracocertesis

A

Between intercostal spaces of 7 and 9 - ventral for find aspiration, dorsal for air -insert cranial to the rib space to avoid the vessels and nerves caudal to the rib

351
Q

What are indications for abdominocentesis

A

Collect abdominal effusion for cytology or relieve signs of dyspnea caused by abdominal effusion

352
Q

What are contraindications for abdominocatesis

A

Coagulopathy

353
Q

Where do you insert the needle for abdominocentesis

A

1-2 cm right lateral to the umbilicus and slightly caudal

354
Q

Where do you insert the needle for abdominocentesis

A

1-2 cm right lateral to the umbilicus and slightly caudal

355
Q

Where do you insert the needle for abdominocentesis

A

1-2 cm right lateral to the umbilicus and slightly caudal

356
Q

What are indications for arthrocentesis

A

Shifting leg lameness, fever of unknown origin (poly arthritis common cause) joint swelling or pain

357
Q

What are contraindications for arthrocentesis

A

Significant coagulopathy or pyoderma over site

358
Q

What are common arthrocentesis sites

A

Carpus, stifle, tarsus

359
Q

What are indications for an endotracheal Wash

A

Collect airway fluid samples for cytology (cats and small dogs)

360
Q

What are contraindications for endotracheal Wash

A

Patient has to be a good candidate for anesthesia

361
Q

What type of catheter do you use for endotracheal Wash

A

Red rubber catheter

362
Q

What are indications for transtracheal Wash

A

Collect airway fluid samples for cytology

363
Q

What are contra indications of a transtracheal wash

A

Don’t use in small cats or dogs (use an endotracheal wash instead) to avoid iatrogenic subcutaneous emphysema and tracheal laceration

364
Q

Do you sedate patients for a transtracheal wash

A

No - cough is good to get a better sample

365
Q

When is a nasoesophageal feeding tube (ne)/ nasogastric tube (ng ) placed

A

Short term less than 7 days for enteral nutritional support in critically ill patients

366
Q

What are contraindications for ne/ng tubes

A

Nasal cavity disease, coagulopathy, vomiting

367
Q

How far should NE tubes go? Ng? How do you check this

A

NE - up to 8th or 9th rib, past base of heart
NG - 13th rib, several inches into lumen of stomach
Confirm placement with radiographs

368
Q

When is an esophagostomy the placed

A

Long term enteral nutritional support for anorexic patients or patients who have limited ability to eat (disease, surgery, etc) - reserved for cats and small to medium dogs

369
Q

What are contraindications for esophagostomy tube placement

A

Esophageal disease / coagulopathy

370
Q

What are common causes of hypercalcemia

A

Lymphosarcoma , anal sac adenosarcma, neoplasia, renal failure

371
Q

Describe now pth acts on bone, kidney and intestines and how that affects calcium

A

Bone - increase osteoclast reabsorption to increase calcium
Kidney - increase calcium reabsorption and phosphorous excretion and increase calcitriol
Intestines - calcinol causes increased calcium and phosphorous absorption

372
Q
  • Calcium leads to - pth
A

Increased calcium leads to decreased PTH

373
Q

Which calcium value do you check to see if Patient is my hypercalcemic

A

Ionized (free) calcium

374
Q

How do you differentiate between prerenal and renal azotemia

A

USG - poorly concentrated is renal

375
Q
  • Disease can occur due to hyperalcenia
A

Kidney disease

376
Q

Why does pu/pd occur

A

Increased water consumption, reduced tubular function, deficiency or impaired response to ADH

377
Q

What are clinical signs of hypercalcemia

A

Pu/pd , anorexia or hyporexia, lethargy, weakness, seizures or muscle twitching, cardiac arrhythmias

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