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Companion Animal Diseases > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

PCV

A

packed cell volume

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2
Q

neutrophils

A

most common; respond to bacterial infections and inflammatory response

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3
Q

lymphocytes

A

infection, chronic inflammation, long term immune response

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4
Q

monocytes

A

bacterial, viral, fungal infections (VF), autoimmune conditions

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5
Q

basophils / eosinophils

A

produce histamine, respond to allergens and parasites

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6
Q

how can you determine anemia in a patient?

A

pcv, hematocrit, MCV and MCHC

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7
Q

normocytic

A

MCV is normal

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8
Q

MCV

A

size of RBCs

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9
Q

MCHC

A

concentration of hemoglobin

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10
Q

normochromic

A

MCHC is normal

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11
Q

leukocytosis

A

increased WBCs, infection/inflammation

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12
Q

leukopenia

A

decreased WBCs

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13
Q

stress leukogram

A

neutrophilia, lymphopenia, and monocytosis
usually as a stress response

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14
Q

thrombocytopenia

A

decreased PLT, due to loss, destruction, or lack of production
could be false due to clumping

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15
Q

thrombocytosis

A

rare, usually as a result of stress

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16
Q

ALP

A

alkaline phosphatase
enzyme, primarily in liver, that helps break down proteins

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17
Q

what does the liver do?

A

filters toxins
produces bile acids to break down food

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18
Q

ALT

A

aminotransferase
primarily liver, also kidneys, heart, muscle, pancreas, spleen, and lungs
catalyzes interconversion of AA’s and oxoacids by transfer of amino groups

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19
Q

GGT

A

gamma glutamyl transferase
primarily found in liver
transfers glutamyl moiety to other acceptors for glutathione recycling, aiding in glutathone production and protection from oxidative stress

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20
Q

AST

A

aspartate aminotransferase
in liver and other vital organs/muscle
catalyzes reaction between AAs aspartate/glumamate
important for AA metabolism

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21
Q

TBIL

A

total bilirubin
byproduct of liver breaking down hemoglobin
excreted in bile, ONLY in liver

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22
Q

what do the kidneys do?

A

filter toxins through urine

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23
Q

BUN

A

blood urea nitrogen
urea is produced by liver as a byproduct of protein digestion and is removed by the kidneys

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24
Q

CREA

A

waste byproduct of wear/tear of muscles and protein digestion
removed by the kidneys

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25
Q

SDMA

A

AA produced by protein breakdown
increased SDMA = decreased GFR

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26
Q

LYTES

A

K, Na, Cl

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27
Q

total proteins

A

ALB and GLOB

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28
Q

ALB

A

protein made by liver to move small molecules through blood (bilirubin, Ca, progesterone, meds)

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29
Q

GLOB

A

helps make up antibodies, liver function, inflammation, clotting (a,b,g)

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30
Q

what is the most radioopaque material?

A

metal

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31
Q

signs of FB obstruction

A

profuse vomiting, inability to keep anything down
diarrhea + blood
painful/hunched posture
inappetence
polydipsia
lethargic
weight loss (usually after 7 days)
bloated/rigid abdomen

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32
Q

reasons an O brings in pt for poss FB

A

O saw pt eat object (not always)
consistent v/d for days
ADR (painful, inappetent, lethargy)

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33
Q

PE findings of a GIFB

A

attitude can be BAR or QAP
painful upon abd palpation
pale gums in severe cases
tachycardia/tachypnea

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34
Q

why would a possible GIFB present with pale gums?

A

the object may press down on the intestines, damaging vessels and sending the animal into shock

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35
Q

other differentials for poss GIFB

A

pancreatitis, gastroenteritis, bacterial/viral GI infection, liver disease, diabetes mellitus, kidney disease, Addison’s, intussusception, neoplasia (cancer)

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36
Q

initial diagnostics for possible GIFB

A

cbc/chem, radiographs
CPL, UA to determine diabetes, AUS

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37
Q

barium

A

radiopaque liquid material safe for ingestion that helps map GI tract

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38
Q

barium study

A

if an obstruction is present, barium gets stuck in the area and highlights in rads

do pre administration rads, 30 mins post, then q1hr until barium is in colon

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39
Q

why do you have to be careful with barium?

A

if aspirated, it will NOT be absorbed and cause permanent damage (lungs)

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40
Q

partial obstruction

A

some material too big to pass out of stomach, moves in/out of way of material moving into duodenum
fabric/hole-y material allows some water/stool to pass

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41
Q

full obstruction

A

no ingesta can pass through stomach/SI
causes significant damage to stomach lining and SI- if severe, intestines can become necrotic

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42
Q

linear obstruction

A

pt eats linear object (string) that gets caught on something in GI tract, impeding movement, but intestines attempt to move it along

causes plication (appears like stretched out fabric)

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43
Q

radiographic finding of a GIFB

A

gas distention in stomach OR before where object is in SI
plication- c shaped SI loops

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44
Q

treatment for a GIFB

A
  1. conservative management: hospitalization and IVF
  2. endoscopic removal: if object is still in stomach and isn’t fragile/dangerous to esophagus, less invasive than sx
  3. sx
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45
Q

surgery for GIFB

A

IVC and IVF started

pre-meds, induction, gas anesthetic maintenance

shaved/cleaned on ventrum from xiphoid process to groin

incision from cranial to umbilicus to just cranial of pelvis

all abd explored, intestines ran from stomach to colon to find FB, palpate stomach

small incision made into stomach or intestines, careful to avoid major blood supply

material removed and incision closed

abd flushed w/ sterile saline then closed

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46
Q

complications of GIFB

A

object may be too dangerous for surgeon to remove

necrosis in area hard to resect

object (linear) may require multiple incisions

dehiscence can lead to septic peritonitis

incisions damage blood supply and later cause necrosis

pet unstable for sx

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47
Q

anastasmosis

A

joining 2 sides of intestine, blood supply, or other body channels

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48
Q

anastasmosis

A

joining of 2 sides of intestine, blood supply, or other body channels

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49
Q

dehiscence

A

opening of incision/wound

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50
Q

enterotomy

A

surgical incision into intestines

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51
Q

gastrotomy

A

surgical incision into stomach

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52
Q

ileus

A

lack of movement of GI tract

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53
Q

necrosis

A

process of cells/tissues dying due to trauma, disease, or lack of blood supply

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54
Q

plication

A

folding of the intestines, usually due to linear FB

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55
Q

GDV

A

gastric dilatation and volvulus

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56
Q

dilatation

A

stomach enlarges due to gas distention

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57
Q

volvulus

A

turning of stomach into abnormal position

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58
Q

what is the mortality rate of GDV?

A

30% with treatment

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59
Q

who is most @ risk of GDV?

A

extra large breed with deep/narrow chest
2x more likely in males
2x more likely in dogs that eat SID
5x more likely in fast eaters

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60
Q

how does a GDV develop?

A

air accumulates in stomach and is unable to escape
as stomach fills, it begins to flip on itself
spleen and stomach share blood vessels, spleen goes with stomach in flip, cutting off blood supply to both
stomach and spleen necrosis if not corrected
stomach may also rupture

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61
Q

clinical signs of GDV

A

severely lethargic
unproductive retching
sudden bloating/bouncy abd
abd pain
restlessness
unable to stand
hypersalivation
pale gums (shock)
tachycardia/tachypnea

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62
Q

PE for a GDV

A

depressed, painful upon abd palpation, tachycardia/tachypnea, “ping” on abd, pt whining or retching

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63
Q

diagnostics for poss GDV

A

radiographs, fluid therapy, pain meds as hypovolemia is likely due to constricted blood vessels
BW can evaluate organ function and severity of hypovolemia

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64
Q

which pain meds should be used for a poss GDV?

A

opioid butorphanol (cardiac friendly), fentanyl or oxymorphone

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65
Q

what are initial tx for a GDV?

A

fluid bolus to correct hypovolemia and shock, decompress stomach using trocarization or OG tube

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66
Q

OG tube

A

pt sedated, measure equine NG tube from nose-cranial last rib, push down L side

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67
Q

trocarization

A

find most tympanic location on L side, clip/clean, use large needle to stab into area and relieve air

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68
Q

what do radiographs look like for GDV?

A

“popeye’s arm”, gas bubble

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69
Q

what will BW show for a GDV?

A

HCT/PCV low due to hypovolemia
CK elevated due to striated muscle damage
K elevated due to cell damage
ALT/AST elevated due to hypoxic damage
LAC high due to hypotension/inflammation

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70
Q

tx for GDV

A

surgery only

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71
Q

surgical procedure for a GDV

A

prep and initial incision for major abd sx
isolate stomach once open
tech @ head with a bucket for drainage
stomach drains through OG tube
rest of abd examined and closed

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72
Q

gastropexy

A

stomach tacked to side of abd wall to prevent GDV (GD can still occur)

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73
Q

3 techniques for surgical gastropexy

A

circumcostal: relies on gastric seromuscular tissue flap passed through tunnel created behind last full rib and sutured to back of stomach

belt loop: seromuscular flap passed through soft tissue tunnel in abd wall

incisional: most common; relies on healing/fusion of edges of gastric seromuscular incision to edges of vertical transverse abd muscle incision

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74
Q

post surgical care for GDV

A

monitored closely for several hours (greatest concerns are blood clots and shock)
fluid maintenance (electrolytes)
pain medication CRI
PCV/TP, MM, pulse, urine
NPO at least 2 days

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75
Q

complications of GDV

A

delayed necrosis of stomach/spleen

blood clots w/ secondary embolisms

persistent hypotension secondary to hypovolemia

cardia arrythmias (VPCs or atrial fibrillation)

aspiration pneumonia secondary to retching

myocardia depressive factor can cause acute cardiac arrest

severe inflammation leading to multiple organ failure

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76
Q

what is the likelihood of GDV for patients with a gastropexy?

A

4%

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77
Q

how can we prevent GDV?

A
  1. gastropexy
  2. reduce stress (esp food related)
  3. feeding and drinking habits
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78
Q

atrial fibrillation

A

irregular/rapid heart rhythm that can lead to blood clots in heart

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79
Q

azotemia

A

elevation of nitrogenous products (BUN), creatinine in blood, or other secondary waste products within the body

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80
Q

CK

A

creatinine kinase; an enzyme mostly in heart and skeletal muscle, small amounts in brain

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81
Q

crystalloid fluids

A

fluid that is an aqueous solution of mineral salts and other small, water-soluble molecules

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82
Q

DIC

A

disseminated intravascular coagulation; serious disorder where proteins that control blood clotting become overactive, usually after injury/cancer/infection

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83
Q

embolism

A

obstruction of an artery, typically by clot of blood or air bubble

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84
Q

gastrectomy

A

removal of all/part of stomach

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85
Q

hypovolemia

A

decreased volume of circulating blood in the body

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86
Q

hypoxia

A

deficiency in amount of oxygen reaching tissues

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87
Q

lactate

A

biproduct constantly produced in body during normal metabolism and exercise; if high –> impaired tissue oxygenation or shock

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88
Q

lower esophageal sphincter

A

muscle ring between esophagus/stomach that controls when material will enter the stomach

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89
Q

MDF

A

myocardial depressive factor; low molecular weight peptide released from pancreas into blood during shock

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90
Q

pyloric sphincter

A

muscle ring between pylorus of stomach and proximal duodenum that controls when material will leave the stomach

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91
Q

seromuscular

A

relating to the serous (surface tissue) and muscular layer of an organ

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92
Q

trocarization

A

procedure where side of abd is prepared and a large needle is inserted directly into stomach to allow air to escape

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93
Q

VPC

A

ventricular premature complexes; extra heartbeats beginning in one of heart’s ventricles, disrupting regular heart rhythm

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94
Q

what anatomy makes up the upper GI tract?

A

mouth, esophagus, stomach, duodenum

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95
Q

what anatomy makes up the lower GI tract?

A

jejunum, ileum, cecum, colon

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96
Q

what part of the GI tract is used primarily for fermentation?

A

cecum

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97
Q

what are the 5 anatomical sections of the stomach?

A
  1. lower esophageal sphincter
  2. cardia
  3. fundus
  4. pylorus
  5. pyloric sphincter
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98
Q

what are the 4 layers of the stomach?

A
  1. lining - mucosa
  2. submucosa
  3. muscularis externa
  4. serosa
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99
Q

what are the 4 parts of the SI?

A

duodenum, jejunum, ileum, cecum

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100
Q

duodenum

A

first section of SI, attached to stomach, proximal duodenum entrance point for pancreatic and common bile ducts; neutralizes stomach acid, mixes enzymes to help break down chyme, and absorbs nutrients

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101
Q

jejunum

A

second section of SI, absorbs sugars, FAs, and AAs

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102
Q

ileum

A

third section of SI, absorbs bile acids, fluids, and B-12

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103
Q

cecum

A

small pouch extrusion between ileum and colon, stores food material where bacteria can break down cellulose

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104
Q

villi

A

folds of intestinal mucosa and submucosa

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105
Q

microvilli

A

finger-like projections on villi and source of nutrient absorption

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106
Q

crypts

A

a gland found between villi in intestinal epithelium; produces stem cells to help repair damaged epithelium

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107
Q

colon

A

ascending, transverse, and descending
removes water, nutrients, and electrolytes from partially digested food
excretes feces out of body

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108
Q

E coli

A

gram (-), rod shaped, normal flora but has some toxigenic types

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109
Q

Salmonella

A

gram (-), rod shaped, with flagella

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110
Q

Clostridium

A

gram +, most anaerobic, rod shaped, can form endospores

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111
Q

Campylobacter

A

gram (-), microaerophilic, S shaped, can be normal flora

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112
Q

how does E. coli cause disease?

A

binds to intestinal lining, produces Shiga toxin, disrupting protein synthesis in epithelial cells, leading to cell death, sloughing of lining
leads to bloody diarrhea

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113
Q

how does Salmonella cause disease?

A

adheres and invades epithelial cells in mucosa and submucosa

attaches specifically to endocytic cells in Peyer’s patches to create inflammation

secretes endotoxin and exotoxin, forces cells to create ethanolamine (food source)

replicates in macrophages

inflammation impairs absorption

diarrhea

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114
Q

how does Clostridium cause disease?

A

produces a spore once in SI or LI

spore produces enterotoxin (+ others)

damages intestinal lining cells

inflammation and sloughing of tissue

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115
Q

how does Campylobacter cause disease?

A

attaches to enterocytes on mucosal lining, releases enterotoxin/cytotoxin

IgA production

increases inflammation and permeability of interstitial fluids into the lumen

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116
Q

what are the clinical signs of bacterial diarrhea?

A

acute diarrhea, +/- blood
mild-severe lethargy
painful abdomen
inappetence
+/- fever and vomiting

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117
Q

what does black/tarry blood in diarrhea indicate?

A

damage is to stomach

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118
Q

what does frank blood in diarrhea indicate?

A

damage to LI/SI

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119
Q

PE for bacteria diarrhea

A

BAR=QAR, lethargic, painful on abd palpation, v/d in room, +/- delayed CRT due to dehydration

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120
Q

how is bacterial diarrhea diagnosed?

A

rule out other causes of diarrhea with fecal float for parasites, rads for abd mass or FB, CBC/CHEM for hepatic/renal/metabolic/endocrine diseases

fecal smear

GI profile (PCR sent out)

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121
Q

how is bacterial diarrhea treated?

A

antibiotics, fluids
- Erythromycin
- Sulfa-Trimethoprim
- Enrofloxacin (aerobic bacteria only)
- Metronidazole

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122
Q

irritable bowel syndrome or irritable bowel disease

A

severe inflammatory response of the submucosal lining in SI/LI

may be idiopathic caused by chronic food allergies/intolerance, bacterial, or parasitic infection

more common in cats

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123
Q

what is the most common type of IBS?

A

lymphocytic plasmacytic enteritis, when lymphocytes infiltrate into submucosa, damage mucosa, and increase permeability, leading to loss of interstitial fluid

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124
Q

what are the clinical signs of IBS?

A

chronic intermittent vomiting +/- diarrhea
lethargy
weight loss
PU/PD
stomach noise (borborygmus)
halitosis and flatulence

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125
Q

PE for IBD

A

BAR-QAR
+/- lethargy
bloating/mild ascites buildup palpable
+/- ropey intestines on palpation
poor haircoat due to impaired absorption

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126
Q

diagnostics for IBD

A

CBC - hypoproteinemia, hypocalcemia, neutrophilia

fecal float/smear to rule out other

AUS - thickening of intestinal wall

exploratory sx with intestinal biopsy (only way to definitively diagnose)

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127
Q

what is the tx for IBD?

A

diet- less carb/lactose/fat, high quality protein

Prednis (ol) one: steriod; BID for 1mo, then decrease by 50% q14 days

Azathioprine: immunosuppressant, must monitor CBC every 2 weeks

Metronidazole: BID for 2-4 weeks then SID

Intestinal protectants: sucralfate, cimetidine

Vitamin therapy: A, D, K, B

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128
Q

hemorrhagic gastroenteritis (HGE)

A

idiopathic, severe, bloody diarrhea, possibly due to hypersensitivity to Clostridium

causes significant damage to intestinal epithelial lining, leads to necrosis of tissue and secondary loss of fluids, proteins, and blood into intestinal lumen

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129
Q

clinical signs of HGE

A

profuse hemorrhagic diarrhea, vomiting, lethargy, anorexia, pale gums

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130
Q

PE for HGE

A

QAR-obtunded
delayed CRT
+/- abd pain on palpation
profuse bloody diarrhea
tachycardia

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131
Q

diagnostics for HGE

A

CBC/CHEM: severe hemoconcentration, neutrophilia, hypoproteinemia, +/- hypoglycemic

LYTES: low

Rads: diffuse ileus and fluid filled loops of bowel

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132
Q

tx for HGE

A

stabilization on IVF or bolus
IV abx, none PO
supportive meds

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133
Q

what is the pancreas?

A

major exocrine organ in mesentery, close to proximal duodenum

2 lobes, each with duct attached to duodenum for enzymes to be released into GI tract

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134
Q

how is the pancreas structured?

A

exocrine - acini
endocrine - islets of Langerhans

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135
Q

acini

A

cluster of epithelial cells in the pancreas that synthesizes, stores, and secretes digestive enzymes

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136
Q

what are the 3 cell types in the pancreas?

A

beta, alpha, and delta cells

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137
Q

beta cells

A

secrete insulin (70%)

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138
Q

alpha cells

A

secrete glucagon (20%); works opposite to insulin, encourages increase in BG concentration

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139
Q

delta cells

A

secrete somatostatin (hinders release of other hormones) and pancreatic polypeptides

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140
Q

how is insulin produced and carried into beta cells?

A

produced in Golgi apparatus, packaged into granules, then carried into beta cells by GLUT2

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141
Q

what happens after insulin enters beta cells?

A

intracellular concentration increases, beta cell membrane depolarizes due to Ca2+ influx, exocytosis of granules

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142
Q

what role does epinephrine play in insulin production?

A

it shuts it down; we want glucose to be free/used, not stored

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143
Q

how does insulin work?

A

insulin allows glucose to be taken up by insulin-dependent tissues (muscle and adipose/fat)

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144
Q

describe what insulin does in response to hyperglycemia

A

insulin is secreted by beta cells

binds to tyrosine kinase (insulin receptors) on surface, leading to phosphorylation

GLUT4 vesicles are released into exc space

GLUT4 binds to glucose and brings it into the cell

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145
Q

Diabetes Mellitus

A

metabolic condition where body does not take up glucose from blood, leading to hyperglycemia

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146
Q

what is a normal BG for cats/dogs?

A

80-120 mg/dL

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147
Q

type 1 DM

A

insulin dependent; requires insulin therapy

beta cells are destroyed due to trauma, autoimmune disease, inflammation, therefore no insulin is produced and no glucose uptake

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148
Q

type 2 DM

A

non insulin dependent; does not require insulin therapy

beta cells produce less insulin, insulin dependent cells respond less, and cells cannot uptake glucose

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149
Q

what type of diabetes will dogs get?

A

type 1

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150
Q

how does DM happen secondary to obesity?

A

cortisol (stress) leads to weight gain due to sugar production, reducing production of insulin, and beta cells are less likely to improve production

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151
Q

diabetic ketoacidosis (DKA)

A

after the body has been hyperglycemic for a long period, tissues are unable to get needed sugar for energy, has to turn to other energy sources

fat in liver is broken down, creating ketones, which decrease the ph of blood, making it acidotic

electrolyte imbalances, cardiac suppression/arrhythmias, renal insufficiency

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152
Q

clinical signs of nonketotic DM

A

PU/PD, weight loss, polyphagia (hunger), sudden cataracts (dogs), dehydration, plantigrade posture (cats)

153
Q

clinical signs of ketotic DM

A

depressed/lethargic, weak and unable to walk, tachypnea, vomiting, sickly sweet breath, +/- diarrhea

154
Q

PE for DM

A

BAR-obtunded
likely obese
lethargic
non painful
+/- cataracts
ataxia (cats) due to weakness
ADR

155
Q

diagnostics for DM

A

CHEM:
elevated BG
+/- elevated K
elevated ALP/ALT/AST
+/- elevated Phos
Falsely low Na

CBC: NSF in nonketotic; if ketotic:
50% nonregenerative anemia
neutrophilia, thrombocytosis

UA: glucosuria, +/- ketonuria, pyuria, and hematuria

156
Q

treatment for nonketotic DM

A

insulin therapy (regular fast-response, NPH/Vetsulin/Prozinc, or Glargine

food therapy

157
Q

treatment for DKA

A

IVF (LRS) to correct dehydration
KCl as CRI
insulin therapy, usually IM q1 hr

158
Q

how can you monitor diabetic patients?

A

Fructosamine level: measures avg BG for 2-3 weeks

BG curve: initial sample, insulin dose, then another sample q2-4 hours

Freestyle Libre: electronic device

Water intake

159
Q

insulinoma

A

beta cell islet tumor that secretes excessive amounts of insulin, causing too much glucose to be taken in by cells, leading to significant hypoglycemia

25% of all ferret tumors

160
Q

clinical signs of insulinoma

A

> 2y, neurologic signs (ataxia, seizures, disoriented, collapse), musculoskeletal signs (weakness, twitching), or GI signs (nausea, vomiting)

161
Q

PE for insulinoma

A

normal unless during an episode
tumors not palpable (may feel enlarged spleen)
alopecia (due to adrenal disease)

162
Q

diagnostics for insulinoma

A

CBC/CHEM: severe hypoglycemia
Rads: rare to see mass, may see enlarged spleen, +/- metastatic nodules in lymph nodes, spleen, or liver

163
Q

treatment for insulinoma

A

hospitalize if in episode, with fluid therapy and restricted activity

surgery to debulk nodules on pancreas, check other organs for metastasis, then measure BG q6-12 hours post surgery via urine

Prednisone or Diazoxide

164
Q

Diazoxide

A

inhibits pancreatic insulin secretion and stimulates epinephrine release

165
Q

prognosis for insulinoma

A

with surgery, the median euglycemic interval is 240 days, and median survival time is 483 days

166
Q

acinus

A

small saclike cavity in a gland, surrounded by secretory cells

167
Q

depolarization

A

cell membrane becomes less negative

168
Q

endocrine

A

glands secrete hormones directly into blood

169
Q

exocrine

A

glands secrete products through ducts opening into epithelium instead of directly in blood

170
Q

exocytosis

A

contents of a cell vacuole are released to the exterior through fusion of vacuole membrane with the cell membrane

171
Q

gastrin

A

hormone that stimulates the secretion of gastric substances into the bloodstream; secreted by stomach wall during digestion

172
Q

islet of langerhans

A

groups of pancreatic cells secreting insulin and glucagon

173
Q

adrenal glands

A

endocrine glands that produce hormones, located in the retroperitoneal space medial kidney; vascularized and innervated

174
Q

what are the 3 layers of the adrenal glands?

A

capsule, cortex, medulla

175
Q

what are the 3 layers of an adrenal gland’s cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

176
Q

zona glomerulosa

A

outermost layer of the adrenal gland cortex, produces mineralocorticoid hormones (aldosterone)

177
Q

aldosterone

A

mineralocorticoid hormone
controls the balance of water/salts in the kidneys by Na+ retention and K excretion

178
Q

zona fasciculata

A

middle and thinnest part of adrenal gland cortex, secretes glucocorticoids and has metabolic effects on several tissues, increasing glycogen synthesis, mobilization of lipids, and protein catabolism

179
Q

glucocorticoids

A

natural form of steroids

180
Q

zona reticularis

A

innermost layer of adrenal gland cortex
primarily produces androgen sex hormones

181
Q

medulla

A

contains chromaffin cells, where norepinephrine and epinephrine are made; controlled by SNS

182
Q

Renin-Angiotensin-Aldosterone pathway

A

hypotension –> kidneys produce renin –> angiotensin converted to angiotensin 1 –> ACE converts angiotensin 1 to angiotensin 2

angiotensin 2 leads to vasoconstriction and increases BP

183
Q

How does angiotensin 2 cause vasoconstriction?

A

it triggers the release of aldosterone and vasopressin from the pituitary gland, causing the kidneys to retain Na+ and excrete K+, leading to water retention

increased blood volume and BP

184
Q

vasopressin

A

antidiuretic hormone, causes kidneys to retain Na+ and excrete K+

185
Q

Cortisol

A

stress hormone, produces in zona fasciculata

controlled by hypothalamus pituitary adrenal axis

counters insulin by encouraging higher BG and stimulating gluconeogenesis

helps with Na+/K+ excretion from kidneys to maintain pH

can cause immunosuppression

186
Q

Addison’s

A

hypoadrenocorticism- the adrenal glands aren’t producing enough cortisol or aldosterone

usually due to immune mediated destruction of the adrenal cortex (or trauma, infection, neoplasia)

causes inability to regulate body ion concentration, kidney function, BG, and BP

187
Q

clinical signs of Addison’s

A

young-middle aged dogs
depression/lethargy
anorexia
vomiting/diarrhea/hematochezia
dehydration
shaking
weak pulse
hypothermia
painful abd
hypoglycemia
hyperpigmentation
alopecia
PU/PD

188
Q

why would an owner bring in a patient with Addison’s? (non crisis)

A

intermittent gastroenteritis (+/- blood)
slow weight loss
lethargy

189
Q

Addisonian crisis

A

hypothermia, lateral, dehydrated, obtunded, weak pulse, hypotension, tachycardic, +/- painful abdomen

true emergency due to shock –> death

190
Q

diagnostics Addison’s

A

CBC: normal leukogram, anemia

Chem: low Na/K ratio, hypoglycemia, azotemia, hypochloremia, hypercalcemia, hypoalbuminemia

can rule out if resting cortisol is >2mug/dL

ACTH stimulation test

191
Q

ACTH

A

adrenocorticotropic hormone

192
Q

the results of an ACTH stim test came back as <2ug/dL for pre and post ACTH. what does this mean?

A

hypoadrenocorticism, needing to be treated with mineralocorticoid/glucocorticoid

193
Q

the results of an ACTH stim test came back as 2-6ug/dL for pre and 6-18ug/dL post ACTH. what does this mean?

A

normal

194
Q

the results of an ACTH stim test came back as >22ug/dL for pre and post ACTH. what does this mean?

A

hyperadrenocorticism (cushing’s), needing to be treated with high dose dexamethasone suppression

AUS

195
Q

treatment for Addisonian crisis

A

correct shock via IVF +/- dextrose, monitor urine for renal failure

administer steroids (Dexamethasone)

196
Q

treatment for Addison’s

A

oral Prednisone BID then SID

Fludrocortisone acetate SID

DOCP q25-28d, with electrolytes rechecked after first few injections then q3-6mo

197
Q

DOCP

A

Percorten-V; mineralocorticoid desoxycorticosterone pivalate

198
Q

Cushing’s

A

hyperadrenocorticism; adrenal gland produces too much cortisol and pituitary gland produces too much ACTH

due to either a tumor in adrenal (15%) or pituitary (85%) gland

199
Q

clinical signs of Cushing’s

A

7-12y old dogs
PU/PD
alopecia (flanks)
low distended abd
polyphagia (inc appetite)
hyperpigmentation
muscle weakness/wasting
poor wound healing
calcinosis cutis

200
Q

calcinosis cutis

A

buildup of Ca+ in dermis/beneath skin, leading to firm bumps on skin

201
Q

PE for Cushing’s

A

BAR-QAR
pendulous abd
alopecia
dry skin with nonhealing wounds
usually coming for comorbitities (UTI, hepatitis, DM)

202
Q

diagnostics for Cushing’s

A

CBC/Chem: stress leukogram (leukocytosis with neutrophilia, lymphopenia, eosinopenia), thrombocytosis, increased ALP/CHOL), hyperglycemia

UA SG <1.020 and proteinuria

resting cortisol to rule out

rads/AUS to see enlarged adrenal glands

ACTH stim test and 3 sample DSTs

203
Q

treatment for Cushing’s

A

Trilostane (Vetoryl) to reduce the amount of Cortisol being produced (blocks the enzyme needed to make cortisol in adrenal glands)

must have ACTH stim test 10-14 days after starting/med change, then q3-6mo

204
Q

what is the MST for Addison’s?

A

4.7y

205
Q

what is the MST for Cushing’s?

A

900 days

206
Q

what are the kidneys?

A

2 bean shaped organs, used to filter byproducts and excessive ions/metabolites out of body into urine; also produces hormones to regulate erythrocyte concentration and regulate BP

207
Q

where are the kidneys?

A

it retroperitoneal space in mid lumbar area lateral to main vessels

208
Q

renal capsule

A

tough, fibrous renal capsule envelopes each kidney and provides support for soft tissue

209
Q

hilus

A

concave aspect of kidney where uteters attach

210
Q

cortex

A

contains glomeruli and convoluted tubules

211
Q

medulla

A

loops of henle and collecting tubules, making up renal pyramids

212
Q

corticomedullary junction

A

junction between the cortex and medulla

213
Q

nephrons

A

filtering units of the kidneys
corticomedullary and juxtamedullary

214
Q

corticomedullary nephrons

A

excretory and regulatory functions

215
Q

juxtamedullary nephrons

A

maintain osmotic gradient of interstitial fluid of medulla, from low –> high in outer to inner medulla

216
Q

how do the kidneys work?

A

blood enters via peritubular capillaries, pressure gradient in glomeruli forces solutes out of blood

proximal convoluted tubule reabsorbs fluids and dumps into interstitial fluid

descending loop of henle allows free water passage

distal convoluted tubule secretes K and H, and Na, Cl, and HCO3 are absorbed

collecting duct reabsorbs solutes and water from the filtrate, forming dilute urine

217
Q

AKI (acute kidney injury)

A

sudden damage to kidneys due to trauma, infection, autoimmune conditions, toxins

218
Q

common causes of AKI

A

infections, such as leptospirosis, toxic plants, chemicals/medications, or shock inducing events

219
Q

how does leptospirosis damage the kidneys?

A

bacteria causes Na+ transport disregulation and decreased aquaporin expression in medulla, resulting in polyuria and natriuresis

220
Q

clinical signs of AKI

A

oliguria (sm amounts of urine)
polyuria
painful kidneys
v/d
anorexia
dehydration
fever
lethargy
mouth ulcers
ataxia

221
Q

PE for AKI

A

dry/tacky gums with reduced CRT and exaggerated skin turgor
tachycardic
lethargic
reduced stimuli response

222
Q

diagnostics for AKI

A

CBC: leukocytosis, neutrophilia, anemia, +.- lymphopenia

CHEM: renal azotemia (elevated BUN, CREA), hyperphosphatemia, hypocalcemia, hyperkalemia, metabolic acidosis

UA: significantly dilute or very concentrated, with active sediment

AUS: kidney size

223
Q

tx for AKI

A

hosp on fluids, treatment with abx/antifungals, hemodialysis to flush system and prevent kidneys from further damage, correct shock

224
Q

how does furosemide work?

A

pulls fluid from interstitium into the blood

225
Q

chronic kidney disease (CKD)

A

chronic decline in the population of functional nephrons
GFR no longer adequate to maintain normal excretory function
more common in cats

226
Q

what is the most common cause of CKD?

A

chronic interstitial nephritis (loss of tubules)

227
Q

risk factors of CKD

A

other diseases include hypertension, hyperthyroidism, DM, Cushing’s

high protein diet in cats

> 5y old

228
Q

clinical signs of CKD

A

weight loss, lethargy, PU/PD, lethargy, v/d, dehydration, unkempt coat, oral ulcers, halitosis

229
Q

PE of CKD

A

depressed attitude, unkempt coat, emaciated, +/- heart murmur, kidneys palpable, retinal detachment, uremic oral ulcers (waste products build up in blood)

230
Q

diagnostics for CKD

A

CBC: mild nonregenerative anemia

CHEM: elevated BUN, CREA, SDMA, hyperkalemia, hyperphosphatemia

UA: SG < 1.030

UPC: measures filtration ability of kidneys

AUS: can r/o neoplasia

231
Q

treatment for CKD

A

slow down progression with kidney friendly rx diet

232
Q

structure of bladder

A

thin walled, saclike organ in pelvic canal
connected to kidneys via ureters
expels urine via urethra
contains transitional cells on mucosa layer
apex, body, trigone regions
urethra

233
Q

urethra

A

tube connecting bladder to exterior of body

234
Q

cystitis

A

inflammation of UB
in cats, idiopathic
in dogs, bacterial cause

235
Q

crystalluria

A

crystals in urine

236
Q

uroliths

A

stones in UB

237
Q

FLUTD cystitis

A

feline lower urinary tract disease (FLUTD)
unknown definitive cause, stress can make it worse
can be obstructive (ulcerative) or nonobstructive (non ulcerative)

238
Q

risk factors for FLUTD

A

middle aged, overweight cats
indoor litterbox/no outdoor time
dry food
stressful environments

239
Q

clinical signs of FLUTD

A

stranguria, pollakiuria, painful urination, excessive licking, inappropriate urination, hematuria, +/- lethargy

240
Q

bacterial cystitis

A

affects ~14% of dogs in life
most commonly due to gram (-) bacteria: e coli, staphylococcus, proteus, klebsiella, pseudomonas

241
Q

risk factors of bacterial cystitis

A

recessed vulva, disease like DM, cushings, CKD, neoplasia, back injuries

more likely in females

242
Q

clinical signs of bacterial cystitis

A

stranguria, foul smelling urine, hematuria, cloudy urine, pollakuria, accidents, +/- lethargy and inappetence

243
Q

crystalluria/uroliths

A

concentrates of minerals in urine

244
Q

what are the 4 types of crystals/uroliths?

A

struvite, Ca2+ oxalates, ammonium biurate, cystine

245
Q

struvite

A

magnesium ammonium phosphates; common in dog urine; significant formation due to UTI due to urease producing bacteria

246
Q

Ca2+ oxalates

A

second most common type

due to high Ca2+, citrates, or oxalates in diet and acidic urine

risk factors are high carb diets and obesity

247
Q

ammonium biurate

A

dalmation, eng bulldogs, spanish water dogs predisposed

animals with liver disease

248
Q

cystine

A

rare and genetic predisposition
heavy excretion of AA cystine

249
Q

clinical signs of crystalluria or uroliths

A

straining, hematuria, accidents, foul odor, crying, +/- lethargy and inappetence, polyuria

250
Q

PE for crystalluria/uroliths

A

painful on palpation
sometimes stones palpable
urinating in room
otherwise NSF

251
Q

diagnostics for crystalluria/uroliths

A

UA: proteinuria, hematuria, +/- elevated leukocytes, alkaline urine, +/- bacteria/crystals on sediment

Culture: helps identify most appropriate abx

CBC/CHEM: r/o other PU/PD conditions (in older pts)

rads: radioopaque stones in UB

252
Q

tx for bacterial cystitis

A

abx: clavamox, enrofloxacin, cefpodoxine

253
Q

tx for FLUTD

A

diet change, avoid stress

254
Q

tx for uroliths/crystalluria

A

surgical removal, dietary change to reduce frequency of stone formation

255
Q

urethral blockage

A

most common in male cats because of long urethra

bacterial/inflammatory/urolith blockage of urethra, preventing excretion of urine and causing backflow into ureters and kidneys

decreases backflow into ureters and kidneys, decreasing blood ph and leading to metabolic acidosis

256
Q

risk factors of urethral blockage

A

young-middle aged cats
overweight
dry food

257
Q

clinical signs of urinary blockage

A

lethargy, inappetence, +/- vomiting, painful abd, stranguria, oliguria or no urine, hematuria, crying

258
Q

PE of urinary blockage

A

painfully firm abd w full bladder
hypothermia
penis red/purple
stranguria
tachycardia

259
Q

dx for urinary blockage

A

rads: confirmation of bladder size and check for uroliths, loss of detail in abd presents concerns for ruptured bladder

CBC: nsf

CHEM: elevated BUN, CREA, hyperkalemia, hyperphosphatemia, elevated liver enzymes

UA: r/o bacterial/crystalluria (FLUTD)

ECG: hr and arrhythmias

260
Q

tx for urethral blockage

A

fluids to correct metabolic acidosis
10% Ca2+ chloride if hyperkalemic
sedation, induction, and sx to alleviate obstruction

261
Q

sx for blockage

A

feed ucath through urethra to bladder gently
drain bladder and flush with sterile saline
suture catheter into place hosp > 3 days with cath

262
Q

recovery for blockage sx

A

IVF
pain medications- bup
prazosin to reduce urethral spasms
surgical perianal urethrostomy if cat continues to block

263
Q

urethrostomy

A

reroutes urethra to another location to widen it

264
Q

pyometra

A

emergency infection of uterus
closed: no discharge
open: discharge draining
usually ~1-3 months after heat cycle

265
Q

risk factors of pyometra

A

middle aged- old dogs intact

266
Q

clinical signs of pyometra

A

lethargy, PU/PD, inappetence, v/d, weight loss, vaginal d/c

267
Q

PE for pyometra

A

QAR-depressed
bouncy/firm abd
+/- pale gums and fever

268
Q

dx of pyometra

A

rads: large soft tissue in caudal abd

CBC: leukocytosis with neutrophilia

CHEM: hyperglobulinemia, elevated ALP/ALT/CREA/BUN

UA: proteinuria and bacteria on sediment

269
Q

tx of pyometra

A

sx, with risk of septicemia
IVF to stabilize
pain medications

270
Q

sx for a pyometra

A

remove entire uterus and inspect for any holes to suggest rupture

271
Q

recovery for pyometra

A

hosp for 24 hrs on IVF and pain CRI
O to monitor for inappetence, v, abd distention (septic peritonitis)

272
Q

prognosis for UTI

A

excellent with chronic care

273
Q

prognosis for urethral blockage

A

improved if brought within 12-24 hrs

274
Q

prognosis for pyometra

A

fair, dependent on age, other diseases, length of time, and if septicemia

275
Q

what are the 3 layers of the heart?

A

pericardium (outer)
myocardium
endocardium

276
Q

what are the 3 conduction nodes of the heart?

A

sinoatral node
atrioventricular node
bundle of his-purkinke fibers

277
Q

structure of the pericardium

A

epicardium
pericardial cavity
perietal pericardium

278
Q

pericardium

A

outermost, inelastic, collagen rich fibrous connective tissue surrounding the heart

279
Q

parietal pericardium

A

outer layer of the pericardium, covered in parietal pleura and touching the lungs

280
Q

pericardial cavity

A

middle layer of the pericardium, the space between outer/inner layer; contains serous fluid to reduce friction

281
Q

epicardium

A

inner layer of the pericardium, firmly attached to outer surface of heart

282
Q

myocardium

A

middle layer of the heart, has striated muscle that goes in 3 different directions
thickest part of the heart that allows pumping of blood

283
Q

endocardium

A

innermost layer of the heart, a thin/smooth membrane that lines the inside of the heart and forms the valves’ surface, for protection

284
Q

tricuspid valve

A

between RA and RV, with 3 leaflets

285
Q

pulmonary semilunar valve

A

between RV and pulmonary artery, with 3 leaflets

286
Q

mitral valve

A

between LA and LV, with 2 leaflets

287
Q

aortic semilunar valve

A

between LV and aorta, 3 leaflets

288
Q

atria

A

thin walled sinuses at base (cranial) of heart

289
Q

auricle

A

conical/ear shaped pouch that projects from each atrium

290
Q

right atrium

A

receive blood flow through vena cava

291
Q

left atrium

A

receive pulmonary veins

292
Q

which ventricle of the heart is thicker?

A

left

293
Q

pulmonary trunk

A

only oxygen poor artery in body

294
Q

pulmonary veins

A

drain into LA

295
Q

aorta

A

largest artery in the body that carries oxygenated blood to the tissues via circulatory system

296
Q

sinoatrial node

A

first conduction node to start signal, has automaticity (spontaneous signaling), on lateral wall of RA

297
Q

atrioventricular node

A

second conduction node, on atrial septum of RA

298
Q

bundle of his-purkinje fiber system

A

last conduction node, node is in ventricular septum and fibers reach deep into apex

299
Q

mitral valve insufficiency

A

myxomatous growths develop on the leaflets of the mitral valve, causing thickening and retraction of the leaflets, with small amount of space between atrium/ventricle

chordae tendinae can tear and cause leaflets to lose structure

blood backflows from ventricle to atrium (pressure gradient)

atrium expand due to inc volume

eventually can no longer expand, addl fluid drains into lungs

300
Q

risk factors of mitral valve insufficiency

A

small breeds
~8y old
progression leads to signs of CHF
often no clinical signs present

301
Q

dilated cardiomyopathy

A

ventricular muscles, esp left side, weaken and can no longer contract appropriately- ventricle becomes wider

renin-angiotensin-aldosterone system is set off
- poor blood pressure due to lack of ability to push blood into aorta
- kidneys work harder
- enlarged ventricles to compensate

pressure gets too high and backflows into lungs

302
Q

arrhythmogenic RV cardiomyopathy

A

in boxers specifically, can cause fainting spells and sudden death due to significant tachycardia (400bpm), ending in v fib

303
Q

risk factors of dilated cardiomyopathy

A

diets lacking taurine (grain free)
3-7y old
males more likely
cats

304
Q

hypertrophic cardiomyopathy

A

abnormal thickening of ventricles, altering contractility/relaxation of the heart as it pumps blood

thick muscle leads to loss of lumen space for blood and force of pumping, leading to bp issues

305
Q

risk factors for hypertrophic cardiomyopathy

A

rare in dogs, common in cats
avg 6.5y old
males predisposed 75%

306
Q

congestive heart failure (CHF)

A

point of no return, prognosis is grave-poor
heart can no longer compensate for any changes, and fluid builds up in lungs, ending with pulmonary edema

animal is drowning in own fluids and has poor contractility to pump blood through heart

307
Q

clinical signs of CHF

A

persistent, non-progressing cough
constant panting
resp distress
tachypnea
exercise intolerance
fatigue/lethargy
cyanotic gums
distended abd
coughing blood
collapse

308
Q

PE for heart disease (any)

A

depends on severity, may be NSF other than heart murmur

309
Q

left apical systolic murmur

A

often heart at site of mitral valve, but if louder can hear everywhere

310
Q

right apical systolic murmur

A

tricuspid regurgitation

311
Q

what are the stages of heart disease in dogs?

A

A- high risk
B1- murmur but no enlarged heart
B2- murmur with enlargement
C- clinical signs of heart failure, tx necessary
D- not responding to tx

312
Q

grade 1 murmur

A

low intensity murmur heart in quiet, after auscultation of localized area

313
Q

grade 2 murmur

A

low intensity murmur heart immediately

314
Q

grade 3 murmur

A

murmur of moderate intensity

315
Q

grade 4 murmur

A

high intensity murmur that can be auscultated over several areas without any palpable precordial thrill

316
Q

grade 5 murmur

A

high intensity murmur with a palpable precordial thrill

317
Q

grade 6 murmur

A

high intensity murmur with a palpable precordial thrill that can be heart without a stetchoscope

318
Q

diagnostics for potential CHF`

A

radiographs, vertebral heart score
echocardiogram
- for cats, will identify structure changes
- for dogs, will indicate severity

319
Q

treatment for CHF

A

Pimobendan, Clopidogrel, Enalapril, Furosemide, Spironolactone, Amlopidine

320
Q

pimobendan

A

Ca2+ desensitizer with vasodilator effects to reduce preload (amount of flow into the heart)

321
Q

clopidogrel

A

anti clotting medication for cats only

322
Q

enalapril

A

ACE (enzyme to convert angiotensin 1 –> angiotensin 2) inhibitor and lower BP

323
Q

spironolactone

A

k+ sparing diuretic

324
Q

furosemide

A

loop diuretic that helps with hyperkalemia

325
Q

amlopidine

A

ca2+ channel blocker used for hypertension

326
Q

P wave

A

depolarization of atrial muscle, followed by return to baseline

327
Q

QRS complex

A

activation of his-purkinje system and ventricular muscle contraction

  • ventricles depolarize
  • repolarization of atria at same time
328
Q

t wave

A

ventricular repolarization

329
Q

P-R interval

A

beginning of P wave to beginning of QRS complex; the time re

330
Q

QRS duration

A

spread of impulses throughout ventricles, measure of intraventricular conduction time

331
Q

Q-T interval

A

measured from beginning of Q to end of T wave, measure of ventricular systole and ventricular refractory period

332
Q

what are 2 atrial abnormalities?

A

atrial fibrillation
atrial premature complex (APC)

333
Q

what are 3 ventricular abnormalities?

A

ventricular fibrillation
ventricular premature complex (VPC)
ventricular tachycardia

334
Q

atrial fibrillation

A

lack of P waves and irregular ventricular rate

QRS complexes are normal-slightly different
rapid rate due to marked pulse deficit

can be due to other heart issues or during sx after giving opioids, GI/resp/neuro disease that elevate parasympathetic tone

335
Q

clinical signs of atrial fibrillation

A

predisposed breeds- irish wolfhound, dane, newfoundland, doby

males

lethargic, weakness, exercise intolerance, sycope, coughing, dyspnea, ascites, anorexia

336
Q

physical exam for atrial fibrillation

A

tachycardic and irregular heart rhythm
murmur if heart disease is present
pulse quality: normal-decreased

337
Q

diagnostics for atrial fibrillation

A

ECG determines irregular ventricular rate
24hr holter vest
echo, cbc/chem, BP check, thoracic rads can r/o other causes

338
Q

treatment for atrial fibrillation

A

heart failure meds
mainly for dogs showed hemodynamic issues (flowing blood)
Procainamide

339
Q

APC

A

premature p waves, or differ from normal in size/configuration

usually occur secondary to structural heart disease (enlargement or atria stretch)

if young, usually due to accessory pathways

can result from electrolyte abnormalities, anemia, endocrine diseases, trauma

340
Q

clinical signs of APC

A

atrial dilation
atrial myocardial disease
electrolyte/metabolic disturbances
hypoxia, anemia
fever
high sympathetic tone
males
labored breathing
exercise intolerance
weakness
collapse

341
Q

PE of APC

A

irregular cardiac rhythm with decreased intensity at first sound

soft atrial sound

342
Q

diagnostics for APC

A

ECG
24hr holter test
echo, T4, thoracic rads, cbc/chem for r/o of other

343
Q

tx for APC

A

treat underlying cause first
anti-arrhythmic meds
- beta blockers such as Sotalol, Atenelol, Carvedilol
- Ca2+ channel blockers such as Diltiazem

344
Q

ventricular fibrillation

A

terminal rhythm + nonexistent heart sounds, pulses, and BP

cardiac arrest

can be secondary to ventricular tachycardia, too deep under anesthesia, or resp arrest/ventilator failure

345
Q

causes of v fib

A

hypoxia
aortic stenosis
heart surgery
drug reaction (anesthetics)
electrical shock
electrolyte imbalances
hypothermia
myocarditis
shock

346
Q

clinical signs of v fib

A

systemic illnesses
previous hx of cardiac arrhythmias
collapse
death

347
Q

treatment for v fib

A

confirm with ECG
CPR + defibrillator to return into normal rhythm
no medications needed

348
Q

VPC (ventricular premature complex)

A

inverted QRS complex

can be caused by cardiac disease, abnormal serum levels of Ca2+ or K+, splenic/GI disease

can lead to hypotension, destruction of cardiac muscle tissue, sudden death

349
Q

clinical signs of VPC

A

weakness
exercise intolerance
fainting
can be asymptomatic
cough or dyspnea if CHF involved
sudden death

350
Q

causes of VPC

A

cardiomyopathy
congenital defects (subaortic stenosis)
chronic valve disease
GDV
traumatic inflammation of heart
digitalis toxicity
heart cancer
myocarditis
pancreatitis

351
Q

PE of VPC

A

dyspnea
collapse
pale gums
abd pain

can happen under anesthesia, indicating pt cannot handle and needs to be woken up

352
Q

diagnostics for VPC

A

ECG
thoracic and abd rads, CBC/chem, and echo to r/o

353
Q

treatment for VPC

A

treat underlying cause
can use similar meds to APCs
hosp if cause is an electrolyte imbalance

354
Q

ventricular tachycardia

A

rapid, regular, or irregular QRS rhythm (300-400bpm)

can be caused by primary cardiac disorders, electrolyte derangements, acid/base imbalances, hepatic/splenic disease, and pheochromocytoma (neuroendocrine tumor)

355
Q

clinical signs of ventricular tachycardia

A

tachycardia
collapse
hypotension
syncope (fainting)
CHF
sudden death

356
Q

risk factor of ventricular tachycardia

A

secondary to DCM in doby, and ARVC in boxers
structural damage to heart, heart failure, or myopathy
systemic disease- hypoxia, anemia, electrolyte/acid-based disturbances, hyperthyroidism
drug reaction

357
Q

PE of ventricular tachycardia

A

lethargic
tachycardia +/- tachypnea
pale gums
collapse in exam room, difficulty getting up

358
Q

diagnostics of ventricular tachycardia

A

ECG
echo, CBC/chem for r/o

359
Q

medications for a dog with ventricular tachycardia

A

lidocaine, quinidine, procainamide

360
Q

medications for a cat with ventricular tachycardia

A

propranolol with small dose of lidocaine

361
Q

AV block first degree

A

longer spacing of P wave from QRS

362
Q

AV block second degree

A

mobitz 1: longer spacing of p wave from QRS over time
mobitz 2: = abnormal spacing over time

363
Q

AV block third degree

A

consistently dropping QRS complexes

364
Q

cause of AV block

A

progressive fibrosis/degeneration of AV node

inflammation/infection of heart muscle or aortic valve, physical disruption of AV node secondary to myopathy, electrolyte abnormalities, or exposure to toxins/meds

365
Q

clinical signs of AV block

A

bradycardia
dogs:
- lethargic
- exercise intolerant
- collapse
- sudden death

cats:
- labored breathing
- collapse

366
Q

PE of AV block

A

BAR-depressed
bradycardic
pale gums
won’t walk

367
Q

risk factors of AV block in cats

A

primary cardiac diseases, systemic/metabolic disease, age-related fibrosis of AV nodal tissue

368
Q

treatment for AV block

A

pacemaker

369
Q

endocardial pacemaker

A

pacemaker lead fed through femoral vein into heart, lead in RV, once in place will feed wire up into jugular vein, jugular then tied off and lead is attached to battery that is placed under the skin

370
Q

epicardial pacemaker

A

open thoracic surgery, using a ventilator
cut open pericardium to form. a window, place leads in proper location on heart, lead wire led out of chest and battery placed under skin

371
Q

sick sinus rhythm

A

heart rhythm where sinus node does not discharge an impulse to trigger heart to contract

heart stops beating

372
Q

risk factors for SSR

A

breeds: westies, dachsunds, schnauzers, boxers, spaniels

females

373
Q

clinical signs of SSR

A

irregular bradycardia
weakness
lethargic
exercise intolerant
collapse
syncope
labored breathing
coughing

374
Q

PE of SSR

A

BAR-depressed
irregular heart beat- arrest, bradycardic, tachycardic
limited movement

375
Q

atropine response test

A

determines if a dog has SSR
atropine normally increases HR; an SSR dog will remain unchanged

376
Q

treatment for SSR

A

pacemaker
medications:
- propantheline
- theophylline
- terbutaline
- hydralazine

377
Q

Which bacteria is the most likely cause of a UTI?

A

E coli

378
Q

what diagnostic test is used to diagnose Cushing’s?

A

LDDS (low dexamethasone suppression test)

379
Q

What 2 parts of the brain help with managing cortisol production?

A

pituitary gland and hypothalamus

Companion Animal Diseases (2 decks)

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