SAMS Midterm Flashcards

(377 cards)

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
What is a severely hypertensive bp range
> 180 mmhg
26
What are the two most common causes of underlying hypertension in cats
Chronic kidney disease ( the most common) and hyperthyroidism
27
What medications can increase blood pressure
Corticosteroids, prion, erythropoietin agents
28
What are the 2 most common underlying causes of hypertension in dogs
Kidney disease (acute or chronic, where as cats are usually chronic) and hyperadrenocorticism (cushings)
29
When should you treat hypertension
Persistent bp over 160 mmhg and causative disease , severe hypertension (>180 mmhg) or evidence of Target organ damage with moderate to severe hypertension
30
What is the first line of treatment for cats with systemic hypertension
Amlodipine - calcium channel blocker (relaxes smooth muscle and cause vasodilation, decreasing bp)
31
When should you recheck blood pressure after treating systemic hypertension with amolodipine and why
7-10 days became that is when drug takes max effect
32
When is ambodipire used to treat hypertension in dogs
When severe >180 mmhg
33
How do Ace inhibitors treat systemic hypertension
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
34
What type of drugs are enalapril and benazepril
Ace inhibitors
35
What is a benefit of Ace inhibitors compared to amlodipine
Ace inhibitors have a more direct effect on the kidneys (can cause a potential drop in GFR and can reduce proteinuria)
36
What is a potential risk of using ace inhibitors
Can cause development of azotemia (increased bun and creatinine /ck) due to decreased glomerular filtration rate
37
What is the list line of treatment for systemic hypertension in dogs (with what exception)
Ace inhibitors except if severe hypertension >180-200 mmhg ( then use amlodipine (a calcium channel blocker) in combo with ace inhibitors)
38
Do Ace inhibitors work to control systemic hypertension
Barely - only reduce bp by 10 or so
39
If you find a dog with Addison’s like lab values (decreased sodium, increased potassium, increased cortisol), what question should you ask the owner
Is the patient on ace inhibitors
40
If Tod is present with severe hypertension, when do you check bp
Even 3 days (7-10 days if no Tod)
41
What goal bp are you truing to reach when feeling systemic hypertension
110 - 140 mmhg
42
With a bp of less than 120 mm hg and clinical signs of disease I what is indicated
Hypotension
43
What is spironolactone used for
Treat hypertension by acting as a aldosterone antagonist and diuretic - reduces sodium and water reabsorption
44
What treatment is used for pheochromocytomas (excess catecholamine production - adrenal tumors)
Alpha adrenergic antagonists because nothing else really works
45
What emergency drugs can be used to treat severe life threatening systemic hypertension and what is the risk
Direct arterial vase dilators ( hydralazine), risk for hypotension (profund quick vasodilation)
46
What is telamisartin
Angiotensin 2 receptor blocker - used for moderate hypertension in cats to reduce proteinuria ( can be used in dogs too); alternative to using ace inhibitors
47
What are two examples of alpha adrenergic antagonists
Phenoxybenzamine and prazosin
48
How does telmisartan work
Inhibits RAAS by blocking action of angiotensin 2 (blocks vasoconstriction and aldosterone production)
49
What is used to that severe life threatening hypertension
Direct arterial vasodilators (hydralazine and sodium nitroprusside)- only use in emergencies due to risk of profound hypotension; monitor with arterial line
50
Spirolectore is - sparing and useful to treat -
Potassium sparing and used to treat hyperaldosteronism
51
What are differentials for petechia
Def: Red or purple spots indicating hemorrhage under the skin Diff: thrombocytopenia, endothelial dysfunction, thrpmbocytopathia
52
Loss than 50,000 platelets leads to concerns for
Spontaneous hemorrhage
53
Decrease albumins and increase globulins often indicate
Inflammation
54
What are 4 causes of thrombocytopenia
Decreased production, immune mediated destruction, consumption, sequestration
55
What tick transmitted disease can lead to pancytopenia (bone marrow disease)
Ehrlicia Canis - rickettsial disease
56
What on a blood smear can indicate Ehrlicia Canis (but does not rule it out if it is not there)
Morula in monocytes plus clinical findings
57
What is CME in regards to ehrlicia Canis? How and where is it transmitted
Canine monocytic erhlicosis - transmitted by the brown dog lick and found in warmer climates
58
What is the name of the brown dog tick
Rhipecophalus sanguireus
59
Describe the acute phase of E. Canis - when does it occur
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)
60
When will the acute phase of E. Canis recover
May spontaneously recover after 2-4 weeks will eliminate infection or remain subclinically infected
61
Describe the chronic phase of E. Canis infections
Panculopenia due to bore marrow hypoplasia, marked lymphocytosis , bone marrow plasmacytosis
62
How do you diagnose E. Canis infection
Morulae visualized in monocytes or lymphocytes on blood smear - harder with chronic infections better with splenic or lymph node aspirates
63
Antibody testing indicates - but - not _
Indicates exposure but not active infection
64
What is the serological gold standard to diagnose E Canis
Indirect immune fluorescent antibody test (ifa) - IgG antibodies reliably indicate exposure L2 consecutive tests 7-14 days apart best to determine acute nation)
65
What suggests an acute and active infection of E. Canis
Four fold increase in ig G antibodies between 2 consecutive IFA tests
66
Whole blood PCR is more sensitive for _infections while serology is more sensitive for - infections
Whole blood pcr - acute infections (because DNA is still present) Serology - chronic infections
67
What is the treatment for E-canis
Doxycycline -improvement after 24 - 48 hours
68
What breed is more sensitive to E. Canis infections and have a worse prognosis
German shepards
69
What is transmitted by the lone star tick and causes monocytic ehrlichiosis in humans
Ehrlicia Chaffeenis - rarely causes clinical signs in dogs but dogs can be a reservoir for infection to humans
70
What are differentials for joint effusion and lameness
Polyarthritis - either erosive or nonerosive (idiopathic versus septic)
71
What are differentials if a morula is found in a neutrophil ( specifically granulocytes) on a blood smear
Anaplasma phagocytophilium or erhlicia ewingii (granulocytes)
72
Both A. Phagocutophilium and E. Ewingii cause - and can be treated with - , how can you differentiate between the two
On cause polyarthritis and can be treated with doxycycline , differentiate with PCR or serology
73
What is transmitted by the lone Star tick and cause granulocytic erhlicolisis (replicates in neutrophils )
Ehrlicia ewingii
74
A. American is the
Lone star tick
75
Describe clinical signs of E. Ewingii
Acute infection 3-4 weeks after inoculation, causes polyarthritis, fever, lymphadenomegaly, etc and often a milder infection compared to E. Canis
76
What is transmitted by ixodes tick, is commonly seen in infections with Lyme disease and causes granolocytic anaplasmosis
Anasplasma phagocutophilium - morale seen in neutrophils that can't be differentiated from E. Ewingii
77
What are clinical signs seen with A. Phagocutophilium infections
Often see no signs, will not cause chronic infections, can cause nonspecific signs like fever/ lymphadenomegaly and polyarthritis
78
What is transmitted by Dermacentor tick (American dog tick )
Rocky Mountain spotted fever - Rickettsia ricketsi
79
Describe what happens with RMSF and what you might see clinically
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
80
Which organs are most affected with RMSF
Skin, brain, heart, kidneys
81
Describe the progression of RMSF
Progresses rapidly over 2-14 days
82
How do you diagnose and treat RMSF
Diagnose with serologic testing (ifa), treat with doxycycline, purebreds most affected ) may clear infection spontaneously
83
What protozoan infection is must spread by ingestion of A. Maculatum the gulf coast tick
American canine hepatozoonosis - caused by hepatozoon Americanum
84
What clinical signs do you see with hepatozoon Americanum
Severe muscle wasting, hypesthesia, stiff gait _ signs wax and wane with severity
85
What on CBC could indicate infection of H. American
Elevated leukocytes, increased alp, hypoglycemia
86
Where do signs occur with H. Americanum infection
Periostea bore proliferation along the proximal limb bones
87
How do you diagnose H. Americanum
Blood smear, skeletal muscle biopsy, whole blood pcr
88
How do you treat H. Americanum
TCP - TMS , clindamycin, pyrimethamine and then decoquinate to prevent clinical relapses (which are common)
89
Describe Babesia Canis
Large piroform shaped Protozoa existing in single or paired erythrocytes usually transmitted by the brown dog tick (R. Sanginueus)
90
The differentiate between Babesia Canis and Babesia gibsonii
Small Protozoa in single entrochtes (Babesia Gibson I)
91
What are clinical signs of uncomplicated Babesia
Thrombocytopenia and imha
92
_ Have a high prevalence of B. Gibsoni without clinical signs likely due to
Pitbuls, transmission by bite wounds
93
How do you diagnose Babesia infections
PCR
94
How do you treat Babesia infections
B. Canis - imidocarb B, gibsonii - Azithromycin (a macrolide)
95
Define anemia
Reduced oxygen carrying capacity from insufficient hemoglobin and red blood cell mass in the vessels
96
What are 3 general causes of anemia
Loss, destruction Or hypoplasia (not making new RBCs)
97
Destruction and lack of production tend to cause more _ signs
Gradual signs and changes - ABCs last in blood for 7 weeks (loss is usually more of a rapid and severe change)
98
How do you confirm anemia
PCV and TS - CBC is a sample and cant tell you how much blood is actually in the patient
99
What cause of anemia can not be detected by or confirmedwith bloodwork
Rapid blood loss - because hct and PCV are percentages of RBC in blood and there will be minima changes immediately after blood loss
100
Can a dog still be anemic with a normal PCV and hct
Yes - if caused by rapid blood loss (takes a few hours)
101
If you give a shock patient fluids after blood loss , what will happen
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 )
102
Describe the PCV and TS result of anemia due to bloodloss
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
103
Describe PCV and TS with anemia due to destruction , what might the plasma look like
Decreased pcv and normal or increased TS - plasma might be yellow due to RBC destruction
104
Describe PCV and TS with dehydration
Both likely increased (concentrated koolaid)
105
Describe PCV and TS with inflammation
PCV normal, globulins cause an increase in TS
106
Describe PCV and TS with anemia due to lack of production
Decreased POV, normal or increased TS (concentrated koolaid)
107
Describe CBC changes for blood loss anemia - what is important to note
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)
108
Describe a regenerative anemia on CBC and why
Macrocyctic, hypochromic, polychomasia (means a diff sizes and shapes )- immature ABCs are bigger and lighter colored
109
Spherocytes on a CBC / blood smear usually indicate
IMHA - immune mediated anemia due to destruction
110
Describe the CBC of an anemia caused by destruction (like IMHA) - what is the exception
Strongly regenerative response (see other flashcard), informatory leukogram, spherocytes _ Will not be the case if the bone marrow is damaged
111
Describe the CBC of anemia due to lack of production
Pancutopenia ( if bone marrow damaged), non regenerative anemia (no reticulocytes , normochromic normocytic
112
What are differentials for chronic anemia
Parasites , ulcers, cancer
113
What are differentials for acute anemia
Trauma, coagulopathy , cancer
114
Hemolytic anemia is almost always - and can be - or -
Immune mediated usually (other causes are toxins, infections, etc) - can be intravascular or extravasalar
115
How can you differentiate between extavascular and intravascular hemolysis
Extravascular - icterus due to biliary excretion of bilirubin Intravascular - renal excretion of free hemoglobin
116
What are differentials for hypoplastic anemia due to lack of production
Refractory anemias (anemia of chronic disease or inflammation, renal failure, Iron deficiency) or bore marrow disorders
117
Are spherocutes bigger than RBC
No - smaller
118
Nucleated RBC on blood smear indicates
Regeneration
119
What disorder looks a lot like an IMHA
Zinc toxicosis - causes oxidative injury (so a regenerative cremia with low POV and normal TS - destruction)
120
What age group usually sees IMHA
4 years or older
121
Describe signs of zinc toxicosis due to something like a penny
Young, vomiting, regenerative anemia, hyper bilirubinemia, informatory leukogram , mild spherocytodis
122
Agglutination on a blood smear indicates
IMHA
123
How do you treat IMHA
Immune suppression (predrisone) and antitrombosis (either anticoagulants or antipktelets) _but prednisone increases risk of thrombosis so need one of the antithombolics the whole time
124
Bruising, signs of shock and a low pcV and TS indicate what type of anemia
Loss
125
Prolonged pt and PTT increase worry of
Blood loss, spontaneous hemorrange and congulopathies
126
What can you give to a patient who needs clotting factors
Whole blood or fresh frozen plasma
127
Describe an iron deficiency anemia
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)
128
Cushings disease is -
Hyperadrenocorticism - adrenal glands overproducing cortisol
129
What results do u expect in a normal dog given the low dose dexmethasone suppression test
At hour zero, cortisol levels should be over 1, at hours 4 and 8 it should be below 1 due to complete suppression
130
Describe the low dose Dexamethasone suppression test
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
131
What will a LDDST look like if cushings (hac) is very likely
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
132
Differentiate between pituitary dependent and adrenal dependent cushings
PDH - increased ACTH production from the pituitary gland ( pituitary tumor) Adrenal dependent - increased cortisol release from the adrenal gland (adrenal tumor)
133
Can a LDDST tell you which type of cushings the dog has
No-just tells you if cushings is likely
134
What are common signs of cushings in dogs
Pu/pd, increased appetite, non pruitic truncal aloepecia, distended abdomen
135
Describe pituitary dependent Cushings LDDST results
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
136
Can all pituitary dependent cushings be determined by the LDDST
No- only 60% follow the pattern, the other 40% will just look like lack of suppression and will need further testing
137
How to you medically manage pituitary dependent cushings - explain side effects
Trilostane - do not give compounded, give with food to maximize absorption , can cause mild lethargy or huporexia for several days
138
How can you assess if trilostane is working? What is the goal
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)
139
Describe the ACTH stimulation test
Give ACTH which shard cause the adrenal gland to increase cortisol
140
When do you first check trilostane response? Should aw increase the dose if it is not working
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
141
What is the risk of uncontrolled cushings
Puts dog in a hypercoagulable state so the risk of thromboemboli increases
142
Will trilostane make a difference in the tumor on the pituitary when treating for PDH cushings
No-just helps treat the long term effects
143
What is the goal of trilostane treatment and how does that apply to dosing
Control clinical signs - don't adjust dose it signs resolved and cortisol is 1.5 or above
144
What response are you looking for on an ACTH stimulation test
Exaggerated response (above 22) after 1 hour
145
Can you differentiate between the types of cushings with an ACTH stimulation test
No
146
How can you differentiate between types of cushings
Endogenous ACTH or abdominal ultrasound
147
What are the treatment options for adrenal dependent cushings
Trilostane to manage clinical signs or adrenalectomy
148
What result would you expect on endogenous ACTH if adrenal dependent cushings
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
149
What would you see on abdominal ultrasound with pituitary dependent cushings
Bilaterally symmetrical enlargement of the adrenal glands because the problem is in the pituitary making too much ACTH
150
What would you see on abdominal ultrasound with adrenal dependent cushings
A mass in the affected adrenal gland and a normal or small contralateral gland
151
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
No - LDDST has low specificity so potential for false positives
152
Can you have hypercalcemia with Cushings
No
153
If there are no signs of cushings, don't
Don't test for cushings
154
What are differentials for multifocal bleeding
Trauma or coagulopathy/ primary hemostatic disorder
155
What are differentials for prolonged pt and ptt indicating a congulopathy
Anticoagulant rodenticide most likely it values are very high, liver failure and DIC don't usually cause a super high increase (usually mild)
156
Will giving packed RBC replace clotting factors
No - need whole blood or fresh frozen plasma
157
Pt prolongs due to a loss of - while PTT prolongs due to loss of -
Pt - loss of factor 7 PTT - loss of factors 2,9,10
158
When is whole blood good to give
Nupovolemic patient, coagulopathy (except platelet function probably won’t be sustained)
159
When are packed red blood cells good to give
Normovolemic, anemic patients
160
When is frozen plasma best to use
All coagulopathies , anticoagulant rodenticides, hypoproteinemia
161
How long do you commonly give vitamin K
28 days - then recheck pt and ptt
162
What are differentials for petechiation
Thrombocytopenia , thrombocytopathia, endothelial dysfunction
163
Where does spontaneous hemorrhage usually occur and at what platelet number
Skin and git usually - 30,000 to 50,000 platelets concern for spontaneous hemorrhage
164
What are general causes of thrombocytopenia
Destruction , decreased production, consumption, sequestration
165
, Very low platelets (10 - 15,000) indicates
Primary immune mediated thrombocytopenia
166
Why might you see splenomegaly in a case of coagulopathy
Sequestration in the spleen causing a thrombocytopenia
167
What antigen in dogs is know for causing transfusion reactions
DEA - blood type testing
168
What is best to replenish all the lost components of blood (proteins, platelets, clotting factors)
Whole blood - if not available, can combine packed RBC and fresh frozen plasma
169
How do now treat primary immune mediated thrombocytopenia
Immunosuppressive dose of steroids
170
What are reasons why the HCT can progressively drop but TS stay the same
Neoplasia causing proteins to be high or dehudation + lasix
171
With acute hemorrhage diarrhea syndrome (AHDS/HGE) , when does diaries usually resolve
Within 5-7 days
172
Differentiate between vomiting and regurgitation
Vomiting - abdominal contractions , might contain bile, nasuea or salivation Regurgitation - passive, esophageal or thoracic disease
173
A vomit that has a coffee ground appearance likely indicates
Partially digested blood, maybe from ulcers
174
When is bilious vomiting syndrome most likely to occur
In the morning on an empty stomach
175
A thyroid slip is most common in - and increases the concern for
Older cats - concerned for hyper thyroidisn
176
What are differentials for primary GI disease leading to chronic vomiting
IBD, neoplasia, parasitism, idopathic gastritis, chronic gastric foreign body
177
What are extra GI / systemic differentials for chronic vomiting
Hyperthyroidism, chronic pancreatitis hepatobilary disease , CKD, hypercalcemia
178
What are common signs of hyperthyroidism
Left thyroid slip with good appetite and weight loss - does not have to have a thyroid slip
179
Why could hypercalcemia cause chronic vomiting
Because it causes dismotility of the git
180
What are differentials for weight loss with a normal appetite
Enteropathy (IBD, neoplasia), metabolic (hyperthyroidism or diabetes), exocrine pancreatic insufficiency (often have diarrhea as well)
181
Can parasites cause chronic vomiting
Yes - also can cause weight loss with a good appetite
182
What can you look at to assess liver function
Glucose, bun, billirubin, cholesterol
183
What could cause a low albumin and a low globulin
PLE or bleeding/hemorrhage (a PLN would have low albumin but normal to increased globulins)
184
Will you always see malena with GI bleeding
No - only 50% so do a fecal blood test
185
When would you do a hypoallergenic diet trial? How do you do it
Only in stable patients, if suspecting food responsive IBD - put on a strict hydrolyzed or novel protein diet for 3 weeks
186
What is the risk of albumin continually dropping in a PLE
Life twittering effusion can develop - need close monitoring
187
What is the benefit of ultrasound over rads in cases of PLE
Better evaluation of soft tissue and mucosal lining of stomach, git
188
Differentiate between surgical and endoscopic git biopsies
Surgical - full thickness success to al portions of the si Endoscopic - includes mucosa and submucosa, access to only the stomach, duodenum and ileum
189
How do you treat inflammatory bowel disease
Prednisolone (immunosuppressive steroids) - taper once albumin is controlled and signs go away (taper by 25 % every 2-3 weeks to lowest effective dose)
190
What are side effects of prednisolore
Diabetes (monitor glucose - reversible if noticed early ), skin fragility, weight gain , polyphagia, pu/pd / increased risk of infection
191
What is an option other than prednisolone in cats
Bodesonide - locally acting corticosteroid
192
What are 2 antiemetic options for supportive care of chronic vomiting
Cerenia (maropitant) , ondansetron - an combine both if severe refractory vomiting occurs
193
How could you differentiate between IBD and small cell GI lymphoma
PCR - treat the same but add chlorambucil for small cell lymphoma
194
What are chronic vomiting differentials specific to dogs
Dietary indiscretion, bilious vomiting syndrome, pyloric hypertrophy, hypoadrenocorticism
195
Describe small bowel diarrhea
Large volume of feces , normal or increased frequency, weight loss, melena, maybe vomiting
196
Describe large bowel diarinea
Small volume, increased frequency, frank blood (hematochezia), teresmus /straining, pain or urgency to defecate
197
What are differentials for chronic small bowel diarrhea
Primary GI (especially if chronic) - lymphangiectasia ,IBD, parasites, neoplasia, dietary indiscretion Systemic - Addison, exocrine pancreatic insufficiency, hepatobiliary disease, chronic renal failure
198
Differentiate between food allergies and food intolerance
Allergies - immune system involved , reacting against food proteins Intolerance - trouble digesting, immune system not involved
199
Which breed often gets lymphangiectasia ? Describe it
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
What would you expect to see on Chem if muscle washing
Low creatine because it is a by product of muscle metabolism
201
How can you rule out hypoadrenocorticism (addisons disease)
Basal cortisol - rule out if 2 or more, if less than 2 need todo a full acth stimulant test
202
How do you rule out exocrine pancreatic insufficiency
TLI - takes a few day; EPI usual causes an increase in appetite due to decreased absorption
203
How can you rule out or differentiate between lymphangiectasia and IBD
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
Differentiate between primary and secondary intestinal lymphangiectasia and treatment
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
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What ave consequences of PLE
Thromboembolic disease ( hypercoagulae state), vitamin deficiencies und malnutrition , poor encotic pressure leading to effusion, edema, etc
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How do you rule out histoplasmosis
Urine antigen test
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What are differentials for large bowel diarrhea
Histocutic ulcerative colitis (boxer colitis- steroids can make this worse) , IBD, infectious (whipworms in colon), IBS- neoplasia
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What are the 3 types of IBD
Food responsive, antibiotic responsive,steroid responsive
209
Describe the physiology of bilirubin
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
Extravascular hemolysis an lead to an increase in -
Unanjugated bilirubin (hasn’t been conjugated by the liver yet)
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Describe prehepatic hyperbilirubinemia
Before the liver, body breaking down too many RBC (hemolysis) and overwhelming the system
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Describe hepatic hyperbilirubinemia
Breaking down normal amount of RBC but liver is not processing it as well, not being conjugated or excreted into bile
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Describe post hepatic hyperbilinbiremia
Problem after conjugation with getting out of the body, some obstruction between the liver and rectum
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What are differentials for prehepatic hyperbilinbiremia
Hemolysis, anemia, immune mediated (imha), toxin (zinc - penny), post transfusion (lots of old RBC)
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What are differentials for hepatic hyperbilirubinemia (functional problem)
Liver failure - toxins, hepatitis/infectious, cirrhosis (scar tissue), portosystemic shunts (end stage), microvascular dysplasia, secondary injury (hepatic lipidosis), congenital deficiencies ; prognosis really pour
216
What are differentials for post hepatic hyper bilirubinemia
Billiary obstruction - gall bladder mucocele , cholethiasis (gallstones) , pancreatitis, tumors
217
What do orange gums make you suspicious of
Some RBC plus icterus of hyperbilinbiremia - hepatic and post hepatic causes high an list
218
Yellow/ icteric gums make you suscpicious of
Hemolysis - prehepatic hyperbilirubinemia
219
How can you differentiate between causes of hyperbilinbiremia
PCV ICT to check for anemia, chem to check for liver leakage enzymes, ultrasound to check for mucocele
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It you have huperbilirobinemia and see diction of the common bile duct, what do you suspect
Suspect post hepatic
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How long before hyperbilinbirenia resolves
Slow - likes to sit in fit tissue so can still be icteric long after resolving the problem
222
How much hyper bilinbirenia is needed to see icterus
3mg/dl
223
What is the main function of the exocrine pancreas
Digestion and to package digestive ensures in a way to safely get to git without digesting the wrong thing
224
What is pancreatitis
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
What are signs of pancreatitis
Vomiting, diarrhea, abdominal pain (unlikely pancreatitis if not painful) , anorexia, dehydration, lethargy
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Is it super important to confirm suspected diagnosis of pancreatitis
No - treatment is most supportive care of symptoms
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What is the limitation with using biopsy to diagnose pancreatitis
Invasive and may not yet the affected part of pancreas (whole thing not always affected)
228
What could a PLI help you diagnose
Pancreatitis (where as TLI diagnosis epi) - very good screening test
229
How is a PLI (pancreatic lipase immunoreactivity) snaptest helpful in diagnosing pancreatitis
If negative, pancreatitis is unlikely, if positive could be but could also be other things
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If you get a positive PLI can you diagnose the dog with pancreatitis
No - keep diagnostics
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Do signs of pancreatitis wax and wane? Can pancreatitis be non painful
No and not usually no
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What is the treatment for pancreatic
Supportive are while body heals itself
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What is really important when treating pancreatitis
Managing pain
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The gut heals faster with -
Food - place NG tube when stable
235
What is the most common endocrinopathy of cats
Hyperthyroidism - occurs in 15% of cats over 10 years old
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What is hyperthyroidism
Excess production of T4 and T3 (which suppresses TSH)- due to thyroid adenomas, adenomatous hyperplasia or rarely carcinoma
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What are the goals of hyper thyroid treatment
Achieve euthyroidism and avoid worsening kidney function bu making more hyper or hypothyroid
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What are the goals of hyper thyroid treatment
Achieve euthyroidism and avoid worsening kidney function bu making more hyper or hypothyroid
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How does hyperthyroidism affect kidneys
Hyper thyroid increases GFR which decreases creatinine - when you treat hyperthyroid you often unmask CKD in cats so warn owners
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What will always go dan when treating hyperthyroid in cats? What will go up when treating CKD
GFR will always go down, CK will go up when treating CKD
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How can you medically manage hyperthyroid in cats
Methimazole - cheap, effective long term, reversible, oral or transdermal application, tumors will still progress to carcinomas and methinazole resistance can occur
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What are side effects of methimazole
GI signs, hepatotoxicity, facial pruritis - usually seen in first few months
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How do you monitor metimazole
CBC / Chem and T4 in 2-4 weeks
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Describe surgical thyroidectomy for treatment of hyperthyroidism
Risk of hypothyroid and hypoparathyroid, recurrence ever when done bilaterally
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What is the treatment of choice for hyperthyroidism ? Describe it
Radioiodire - 95% efficacy with one treatment, destroys abnormal thyroid tissue - need 2 week at home isolation
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When are methimazole trials done before radioiodine treatment in hyperthyroid cats
In cats who are azotemic at diagnosis to monitor CK values
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Describe nutrition therapy for hyper thyroid cats
Low iodine diet, must be the only thing the cat eats - goal is to lower the thyroid hormone levels
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What are the benefits of feeding low iodine diets to hyperthyroid cats
Normalize T4, signs improve in 4 weeks , CK decreases
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When is it best to use nutrition therapy to treat hyperthyroid in cats? When is it hard
Best - cat can't tolerate methinazole, concurrent disease or renal insufficiency Hard - indoor/outdoor cats, multi households
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What is the most common case of hypothyroid
Iatrogenic when treating hyperthyroidism
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How often does hypothyroid occur when treating hyperthyroid
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
Why is hypothyroid caused by treating hyperthyroid bad
More likely to be azotemic, decreased GFR, decreased survival - goal is euthyroid!
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What are clinical signs of hypothyroid
Weight gain, decreased appetite (opposite of hyperthyroid), pu/pd
254
Which is a more accurate test for hypothyroid
Free T4 _ total T4 made more inaccurate by non thyroidal illness (like in cats with CKD have low T4)
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What indicates subclinical hypothyroidism
Elevated TSH with normal T4
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What is the most sensitive test for hypothyroidism
TSH
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When do you monitor post treatment of hyperthyroid
1 month - check for resolution of hyperthyroid 3 months - detect hypothyroid 6 mantas - determine renal function
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When do you treat hypothyroidism and how
Permanent it present at 6 month check - treat if new or worsening azotemia; treat with levothyroxine to increase GFR and improve kidney anchor
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- Thyroid is most common in dogs 1 - thyroid is most common in cats
Hypothyroid - dogs, hyper thyroid - cats
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Describe total T4 as a diagnostic test
Very sensitive for diagnosing hypothyroid but not specific (false positives are common)
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What is the best thyroid function test available
Free T4 - highly sensitive and specific
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Testing TSH is used for
Diagnosing hypothyroid early - insensitive (only elevated in 60-75 % of hypothyroid) very specific
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What thyroid hormone values absolutely confirm hypothyroid
Low TT4 and free T4, high TSH
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TSH is produced by the - and inhibited by _ produced by the thyroid
TSH produced by the military and inhibited by thyroid hormones T4 and T3
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What are common signs of cushings
Pu/pd, weight gain, pot belly, polyphagia
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Will a hypothyroid dog have pu/pd
No never
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What are clinical signs of hypothyroid
Overweight, lethargic, exercise intolerant, non pitting edema causing a sad face, double chin look
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What are clinical signs of hyperthyroid
Thin, tachycardia, too much energy, trembling
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Why could a hypothyroid dog have an elevated TT4
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)
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Why could a hypothyroid dog have an elevated TT4
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)
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What kind of drugs can lower T4 making it look like hypothyroid
Phenobarbital, sulfonamides, glucocorticoids, NSAIDs
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What breed may have lowered T4
Sighthounds / greyhounds
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How do you treat hypothyroidism? How should you monitor
Levothyroxine - recheck signs 8 weeks later, 4 cars after giving the pill the T4 should be in the high normal range
274
What value other than TSH is commonly high with hypothyroid dogs
Cholesterol
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Can you use free t4 alone to diagnose hyperthyroid in cats
No - non thyroidal illness can falsely increase it
276
If TSH is normal, the cat is likely not
Not hyper thyroid
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What liver enzymes represent hepatocellular injury
Alt and AST
278
What liver enzymes represent cholestasis /enzyme induction
Alp and GGT
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What liver enzymes indicate impaired liver function
Bilirubin, albumin, glucose, bun, cholesterol
280
Describe alt and reasons it would be increased
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
Define cholestasis
Decreased bile flow
282
The alp value is a combination of
Liver, bone and corticosteroid isoenzymes
283
Increased alp on be induced by what drug
Phenobarbital
284
What disease in cats can cause increased alp and GGT
Hepatic lipidosis
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What can cause an increase in bilirubin
Hemolysis, bile tract disease and liver dysfunction
286
What could cause albumin to be low
Low albumin indicates severe liver dysfunction as long as git and kidney loss are ruled out
287
When does glucose decrease with liver injury
Decreased when over 75 % of liver function is lost
288
What could cause bun to decrease
Decreased from PSS or chronic liver disease
289
What to prolonged clothing times indicate
Significant hepatic disease or factor consumption
290
What is the most sensitive liver function test
Bile acids - use to screen for loss of hepatic function or for PSS
291
When are bile acids contraindicated
If hyperbilinbiremia or jaundice
292
What is the most common cause of abnormal liver enzymes
Secondary to non hepatic disease (drugs, endocrine disease, dental disease, neoplasia, etc)
293
When shard you investigate abnormal liver enzymes further
If alt is greater than twice Normal over several months, non hepatic causes ruled out or unexplained resistant elevation lasting 6-8 weeks
294
What is the main stay of immunosuppressive therapies
Glucocorticoids - prednisolone and dexmethasone
295
What are side effects of glucocorticoids
Pu/pd, panting, polyphagia , muscle atrophy, weakness - can induce inorganic cushings or amicably increase liver enzymes (alp)
296
What are contraindications of steroids
Diabetes mellitus, infection, hyperadenocaticism, NSAID therapy
297
What is the second line therapy for IMHO, IMTP, etc
azothioprine - glucocorticoid sparing effects, taper after prednisone!
298
What is diabetes mellitus
A problem with insulin - either a lack of production or lack of response, characterized by hyper glycemia
299
What is the problem with not having insulin
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
Besides glucose, what else does insulin bring into the cells
Potassium and phosphorous
301
When you give insulin, what will increase in the cell
Potassium, glucose, phosphorous
302
Differentiate between type 1 and type 2 diabetes
Type 1 - lack of insulin production by Beta cells Type 2 - resistance to the effects of insulin
303
Describe the body's response to various glucose states
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
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If insulin - then glucagon will -
If insulin increases, glucagon will decrease and vice versa
305
What is plan B when there is no insulin
Fatty acids get converted to ketones - not as efficient Evers sure, less ATP, the liver cant use ketones but the brain can
306
Are ketones always bad
No- sometimes can be good
307
What are the 3 ketones (which are acids)
Acetone, acetoacetate, betahydoxy butyrate
308
What is enough to diagnose keto acidosis
Diabetes melliits and acidosis with no other cause
309
Why does keto acidosis occur with DM
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
How do you treat DM? How do you treat dka?
Give insulin ! Reverse the ketoacidosis by feeding the cells
311
Differentiate between types of insulin
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
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Why is insulin intentionally short acting
Because once glucose changes it helps to be able to respond quickly
313
What's the difference in goals when treating DM and DKA
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
What are the components of total body water (70%)
Extracellular - interstitial or intravascular Intracellular ( 66%)
315
Describe the Sodium and potassium levels inside the cell, outside the cell?
Inside cell - high potassium, low sodium Outside cell - high sodium, low potassium
316
Describe the sodium and potassium in replacement and maintenance fluid
Replacement - high sodium low potassium Maintenance - low sodium high potassium
317
What's the difference between a balanced and unbalanced
Balanced - similar to Extracellular fluid Unbalanced - too much chloride compared to ecf
318
Fluid tonicity indicates
How salty fluid is
319
When is rehydration typically performed
Corrected over 12-24 hours - faster if renal injury or azotemia because you want to prevent further damage , slower if cardio disease
320
Would you give a fluid bolus for dehydration
No - dehydration occurs too an correct slowly, only give bonus to hypovolemic patients or shock patients
321
What is maintenance fluid rate
30 - 60 mL / day, neonates 80 - 120 ml/day
322
What are potential complications of fluid therapy
Electrolyte imbalances , edema or pitting edema, iatrogenic CHF, phlebitis
323
What is the last sign affected by giving fluids
Lungs - the filtering organs affected first (kidneys, liver
324
What are the possible signs of fluid overload
Naseua , loss of appetite, regurgitation, hard swallowing, extended neck
325
When should you discontinue IV fluids
When patient eating and drinking
326
A high UPC ( urine protein to creatinine ratio) indicates
Glomerular disease
327
A low UPC indicates
Tubular disease
328
What are common presentations of a uremic crisis
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
Differentiate between AKI and CKD
- 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
What are common findings of CKD with acute kidney injury or exacerbation for other reasons
Dehydration, anorexia, vomiting, weakness, lethargy
331
What are complications of CKD
Hypertension (then concurrent retinal damage ), secondary UTI
332
How do you treat CKD with acute exacerbation
Correct dehydration (otherwise kidney damage increases), treat symptoms and correct any comorbidities
333
Describe diuresis in terms of CKD and treatment
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
How do fluids treat CKD
They don't! They treat dehydration and hypovolemia - fluid overload in CKD patients can actually be really bad
335
Dehydrated parents with CKD should
Have their dehydration corrected aggressively then stopped quickly once fixed (in 8 - 12 hours)
336
What is the only kind of azotemia that is corrected with find therapy
Prerenal
337
Rehydration should be done using - and maintenance should be done using -
Rehydration - balanced electrolyte solution like LRS (lower in chloride and better for the kidneys) Maintenance - low sodium find like half saline, discontinue gradually
338
What are two at home treatment options for CKD patients if voluntary water intake is insufficient
Subcutaneous fluids or feeding tube placement (that is not used for feeding)
339
What is a can of subQ fluids in a CKD patient
High in salt - makes kidneys have to work harder
340
What is part of the laver urinary tract
Bladder, urethra, prostate
341
What are recurrent LUT signs
Hematuria, strangeruria (pain on urination), pollikuria (urinating frequent small amounts )
342
What meds are good for treating UTIs
Penicillins - tetracyclines don't reach high concentrations in urine
343
Differentiate between complicated and uncomplicated UTIs
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
What do you use to treat complicated UTIs caused by prostatitis
Fluroquinolones like enrofloxacin
345
What ave indications for a bone marrow aspirate
Unexplained thrombocytopenia or non regen anemia, staging of neoplasia, investigation of atypical cells, checking iron stores
346
What are 3 possible sites for a bone marrow aspirate
Iliac crest of the pelvis, trochanteric fossa of the femur, greater tubercle of humerus
347
Why do you put EDTA through the bone marrow sampling needle
To prevent clotting of blood
348
What are indications of a thoracocentesis
Collect pleural effusion for cytology or relieve clinical signs of dyspnea caused by pleural effusion or pneumothorax
349
What are contraindications for thoracocentesis
Coagulopathies unless a hemothorax caused by a coagulopathu
350
Where do you insert the needle for a thoracocertesis
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
What are indications for abdominocentesis
Collect abdominal effusion for cytology or relieve signs of dyspnea caused by abdominal effusion
352
What are contraindications for abdominocatesis
Coagulopathy
353
Where do you insert the needle for abdominocentesis
1-2 cm right lateral to the umbilicus and slightly caudal
354
Where do you insert the needle for abdominocentesis
1-2 cm right lateral to the umbilicus and slightly caudal
355
Where do you insert the needle for abdominocentesis
1-2 cm right lateral to the umbilicus and slightly caudal
356
What are indications for arthrocentesis
Shifting leg lameness, fever of unknown origin (poly arthritis common cause) joint swelling or pain
357
What are contraindications for arthrocentesis
Significant coagulopathy or pyoderma over site
358
What are common arthrocentesis sites
Carpus, stifle, tarsus
359
What are indications for an endotracheal Wash
Collect airway fluid samples for cytology (cats and small dogs)
360
What are contraindications for endotracheal Wash
Patient has to be a good candidate for anesthesia
361
What type of catheter do you use for endotracheal Wash
Red rubber catheter
362
What are indications for transtracheal Wash
Collect airway fluid samples for cytology
363
What are contra indications of a transtracheal wash
Don't use in small cats or dogs (use an endotracheal wash instead) to avoid iatrogenic subcutaneous emphysema and tracheal laceration
364
Do you sedate patients for a transtracheal wash
No - cough is good to get a better sample
365
When is a nasoesophageal feeding tube (ne)/ nasogastric tube (ng ) placed
Short term less than 7 days for enteral nutritional support in critically ill patients
366
What are contraindications for ne/ng tubes
Nasal cavity disease, coagulopathy, vomiting
367
How far should NE tubes go? Ng? How do you check this
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
When is an esophagostomy the placed
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
What are contraindications for esophagostomy tube placement
Esophageal disease / coagulopathy
370
What are common causes of hypercalcemia
Lymphosarcoma , anal sac adenosarcma, neoplasia, renal failure
371
Describe now pth acts on bone, kidney and intestines and how that affects calcium
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
- Calcium leads to - pth
Increased calcium leads to decreased PTH
373
Which calcium value do you check to see if Patient is my hypercalcemic
Ionized (free) calcium
374
How do you differentiate between prerenal and renal azotemia
USG - poorly concentrated is renal
375
- Disease can occur due to hyperalcenia
Kidney disease
376
Why does pu/pd occur
Increased water consumption, reduced tubular function, deficiency or impaired response to ADH
377
What are clinical signs of hypercalcemia
Pu/pd , anorexia or hyporexia, lethargy, weakness, seizures or muscle twitching, cardiac arrhythmias