Exam 2 Flashcards
(181 cards)
1
Q
How much blood enters the lungs from the right ventricle? A. 25% B. 66% C. 100% D. 0%
A
C. 100%
2
Q
How big is a pulmonary?
A. Diameter of 1 RBC (10ums)
B. Diameter of human hair (17- 180um)
A
A. Diameter of 1 RBC (10ums)
3
Q
Look at the slides 5-13/1
A
.
4
Q
What are the 5 predisposing factors for decreasing functional residual capacity?
A
– Positional changes. – Fasting. – Rumen or gastrointestinal distention. – Species. – Pregnancy.
5
Q
What the mechanisms that can decrease functional residual capacity? (3)
A
– Atelectasis (lung collapse).
– Increased thoracic or abdominal blood volume
– Loss of diaphragm tone at end exhalation.
6
Q
Look at slide 15/1
A
.
7
Q
KNOW THESE 4
What are the four types of hypoxia?
(WILL BE ON EXAM, KNOW/MEMORIZE THEM!!!!!!!!!!)
A
– Hypoxic hypoxia.
– Anemic hypoxia.
– Circulatory hypoxia.
– Histotoxic hypoxia
8
Q
What is the definition of hypoxia?
A
Abnormally low partial pressure of O2 in tissues. From low oxygen delivery (D02)= CO x CaCO.
9
Q
What is the definition of hypoxemia?
A
Abnormally low partial pressure of 02 in arterial blood (Pa02< 60mmHg)
10
Q
What are the five causes of hypoxemia?(All are assoc. w/ hypoxic hypoxia)
A
– Hypoventilation – low fractional inspired oxygen concentration – ventilation perfusion mismatch – anatomical shunt – diffusion impairment
11
Q
What can cause hypoventilation? (4)
A
*inverse relationship between Va and PaCO2
– anesthetics which depresses Central Drive – damage to chest wall – paralysis of respiratory muscles – high resistance to breathing (slide 17/1)
12
Q
What is apparatus dead space? What is the issue this?
A
Apparatus dead space is the space that is taken by the breathing apparatus and doesn’t reach the animal. The issue is that you need to calculate for apparatus densities when figuring out the tidal volume for an animal so it gets full ventilation.
13
Q
How do you minimize the apparatus dead space?
A
Can cut the tube
14
Q
What is functional residual capacity?
A
Volume of gas remaining in lungs after normal expiration.
15
Q
Do all patients that hypoventilate become hypoxic?
A
No
16
Q
What is hypoventilation?
A
When you slow/stop breathing.
17
Q
With a perfusion mismatch in zone one, what would you expect to see? (3)
A
*collapse
- Alveolar dead space
ventilation
- Lung is ventilated but not perfused
- Normally small component in awake healthy animals
18
Q
With a perfusion mismatch in zone two and three, what would you expect to see?
A
*2:waterfall 3:Distention
- Vertical perfusion
gradient
19
Q
What would you not expect to see with a low V/Q or inadequate ventilation?
A. Dead space ventilation with extremely low V/Q (shunt)
B. Pulmonary edema
C. Pneumonia
D. Atelectasis
E. Expect to see all of the above
A
E. Expect to see all of the above
20
Q
What would you not expect to see with a high V/Q or inadequate ventilation? A. Poor pulmonary perfusion B. Pulmonary thromboembolism C. Expect to see all of the above. D. Wouldn't see any of the above. 
A
C. Expect to see all of the above.
21
Q
What does V/Q inequality impair the lung from doing?
A
It impairs uptake or elimination of all gases by the lung.
22
Q
Why can your CO2 be easier corrected by increasing ventilation versus your PO2?
A
CO2 is 20 times more soluble than O2
23
Q
What is an anatomical shunt, and how does it play a role in hypoxia?
A
It is an abnormal vascular connection between the small pulmonary artery and vein. This causes a direct addition of venous blood to atrial blood across a defect between the right and left side.
These animals respond poorly to added inspired O2.
24
Q
Hypoxemia due to an anatomical shunt is more severe when moving from which side to which side?
A
When moving from right to left.
*It is more common to see a left to right shunt
25
Fick's Law of diffusion 31/1.
.
26
What can cause diffusion impairment that will lead to hypoxia?(3)
Pulmonary fibrosis, decrease in RBCs transit time through capillary (intense exercise), thickening of blood–gas interface (smoke inhalation, oxygen toxicity).
27
What is an example of low partial pressure of inspired oxygen? (Think going to Colorado to play a sport)
Altitude sickness (33/1)
28
What are the two causes of low partial pressure of inspired oxygen?
How does the body try to compensate?(34/1)
Causes:
- High altitude
- Oxygen supply to breathing circuit of anesthesia machine is interrupted
Compensations
- Change in p50 of oxygen dissociation curve
- Shift to the left
- Increase affinity of O2 to Hb
- Hyperventilation (Decreased H+)
- Low 2,3 DPG
29
P(A-a)O2 mmHg >30mmHg=?
P(A-a)O2 mmHg<20mmHg=?
Look at slide 18/1 notetaker notes.
>30=Ventilation: perfusion inequality
| <20=hypoventilation
30
Look at slide 36/1Notetaker notes
.
31
Which of the following is false about brachycephalic syndrome?
A. They have high resistance to breathing.
B. Respiratory muscle fatigue due to hyperventilation (does not maintain a normal PaO2)
C. Hypoxia and Hypercapnia with decompensation may happen
D. Get respiratory arrest
E. All of the above are correct.
B. Respiratory muscle fatigue due to hyperventilation (does not maintain a normal PaO2)
*it does maintain normal PaO2
32
What is the best way to prevent an animal with brachycephalic syndrome from needing CPR?
Prevent excitement (this is done by minimal restraint and possible sedatives)
33
What is the biggest issue involving equine postoperative obstructions?
Resistance to breathing due to being obligate nasal breathers.
34
What is laryngeal paralysis?
Denervation of recurrent laryngeal nerve
35
What are the causes of laryngeal paralysis?(7)(not a big deal)
Idiopathic, trauma, neuromuscular disease, neoplasia, hypothyroidism, neuro/myopathy, congenital.
36
How does laryngeal paralysis cause respiratory disease? (3) (these are important)
1. increase upper airway resistance
2. Increased inspiratory effort
3. Dyspnea, syncope, hypoxia
37
What are you more likely to see in the upper respiratory issue, increased inspiratory prolongation/effort or expiratory prolongation/effort?
increased inspiratory prolongation/effort
38
How does the radius of the airway affect the work of breathing? (IMPORTANT WILL BE ON EXAM)
Decreasing radius will increase airway resistance requiring a more negative intraplueral pressure to be generated. This will increase the work of breathing.
39
If you have a high Reynolds number what is the breathing considered to be?
More turbulent. This also increases the work of breathing
40
What is heliox?
Mixture of oxygen and helium. Creates lower Reynolds number and thus turbulent flow.
41
What type of airflow (Turbulent or laminar) will a tracheal collapse cause?
Will this increase or decrease work of breathing? (48-52/1)
Turbulent
| increase work of breathing
42
Define atelectasis.
| In what type of patients is this an important cause of hypoxemia?
Airless or partly airless state of long leading to alveolar collapse.
Critically ill patients
43
What is the primary cause for lung collapse (atelectasis)?
Surface tension
44
What are the four forces that oppose surface tension?
Transpulmonary pressure, tethering affect of surrounding structures, surfactant, gaseous nitrogen skeleton
45
Look at slides 56-58/1
| What can lead to atelectasis? (7)(think about lung collapse.)
Compression, airway obstruction, alveolar fluid accumulation, alveolar trauma, compromise of palm. perfusion, & absorption atelectasis.
46
What are the causes of atelectasis? (4) (59-62/1)
– inadequate expansion
– anesthesia
– anatomic predisposition
– extramural airway compression
47
What animal is it common to see inadequate expansion?
Large animals
48
What are the three examples of extramural airway compression?
Masses, pleural space disease, diaphragmatic hernia
49
What is pleural space disease?
It is a potential space formed by a parietal and visceral pleura.
50
What are the four things associated with pleural space diseases?
Pleural effusion, pneumothorax, diaphragmatic hernia, neoplasia
51
What is pulmonary edema?
Accumulation of extra vascular fluid within the pulmonary parenchyma or alveoli.
52
What are two things that can cause pulmonary edema?(67/1)
High-pressure edema and increased permeability edema.
53
What is the definition of pruritus/itch?(slide 4/2)
Unpleasant sensation stimulating the desire to itch.
54
True or false: axons that mediate the sensation of pain or itch are myelinated axons (C fibers).
False. The axons are unmyelinated.
55
Where are the cell bodies for itch located? (Pick specific ganglia) (5/2)
Cell bodies for itch are located in the dorsal root ganglia of spinal nerves & the trigeminal (Gasserian) ganglion of CN V.
56
Which of the below is responsible for receiving incoming action potentials and transmitting them to the brain?
A. Trigeminal ganglia on
B. Spinothalamic tract neurons in the dorsal horn
C. Dorsal root ganglia
D. Primary somatosensory cortex
B. Spinothalamic tract neurons in the dorsal horn
57
Which of the following is false referring to itch neurons.
A. they intersect or intercommunication with other morons especially those that mediate pain.
B. Pain often inhibits itch.
C. Opioid pain-relievers can cause pruritus.
D. Noxious temperature changes, both cold and hot, modulate itch perception. (bathing in hot water alleviates poison ivy itch)
E. All of the above are true
E. All of the above are true
58
Look at slide 8/2
.
59
What are the four things pruritus results from?(9/2)(all are diseases)
Skin disease, systemic disease, neuropathic disease, psychogenic disease.
60
What are typical things that your owners will see with pruritus? (6)
Biting, licking, chewing, scratching, gnawing, rubbing.
61
Look at slide 11/2
.
62
What are the trigger factors for pruritus?(9)
Which is the most common?
Allergens, bacteria, yeast, food, irritants, psyche, temperature, humidity, hormones.
Allergens
63
Define threshold (involving itch).(KNOW slide 13/2)
Patients can tolerate a certain load of sensations or pruritic stimuli without becoming itchy.
64
True or false: the threshold is the same for everyone.
False. Threshold varies among individuals.
65
What are the 3 general causes of pruritus in dogs?(KNOW)
Allergy, ectoparasites, infections.
66
What are the four allergy related causes of pruritus in a dog?
Flea allergy, atopic dermatitis, cutaneous adverse food reaction, insect bite hypersensitivity/contact dermatitis
67
What are the five ectoparasite related causes of pruritus in a dog?
sarcoptes, demodex, cheyletiella, lice, chiggers
68
What are the three infectious causes of pruritus in a dog?(slide 18/2)
Pyoderma, yeast, dermatophytes.
69
What are the six questions you would ask to characterize pruritus?
* What body sites?
* Any seasonality?
* How intense?
* Which came first: the itch or the skin lesion?
* Age of onset?
* Any helpful treatments?
70
Name cause of pruritis/itch at sites. (specific) 1.Caudal dorsum, 2. Elbows & ears, 3. feet licking/chewing.
Look at slide 21-23/2
CD=flea allergy
EE=Sarcoptes
FL/C=food allergy or atopy
71
What are the three diseases that are the most severe when it comes to pruritus?(Slide 22/2)
Scabies, flea allergy, food allergy
72
How is feline pruritus different from canine pruritus?(4)
– Owner might not recognize the problem.
– Body localization is not as distinctive.
– skin lesions are different
– Rarely: excoriation, lichenification, hyperpigmentation
73
What are the three Allergy related causes of pruritus in a cat?
Flea allergy Atopy
| Food allergy
74
What are the five Ectoparasites related causes of pruritus in a cat?
Notoedres, Demodex gatoi, Cheyletiella, Ectopic ear mites, Fur mite
75
What are the three Infections related causes of pruritus in a cat?
Pyoderma: rare
Yeast
Dermatophytes
76
What are the five things that should be done to sort out all causes of pruritus the first office visit? (slide 26/2)
Good history, good physical exam, derm diagnostics, therapeutic plan, future plan and reassessment
77
Define alopecia.
Partial or complete absence of care from areas of the body where it normally grows.
78
What are the inflammatory diseases that affect the hair follicle? (3) (slide 30/2)
Folliculitis/Pyoderma, ringworm, demodex.
79
What are the non-inflammatory diseases that affect the hair follicle? (2)
endocrine and follicular dysplasia
80
What are your four types of hair? Describe each. (Slide 31/2)
rimary/guard: course, stiff; often longer
secondary or down/undercoat: finer and growing from a more superficial follicle than a guard hair.
sinus: vibrissae or whiskers. Have an endothelium-lined blood sinus between the inner and outer layers of the dermal portion of the follicle with a rich nerve supply.
Tylotrich: special hairs scattered among other hairs. Hair follicles are larger & have a ring of neurovascular tissue around them. Act as rapid-adapting mechanoreceptors.
81
Which of these is false referring to hair cycles?(32/2)
A. Cycles vary with species, breed, body site, type of hair.
B. It can be influenced by systemic factors especially nutrition.
C. Telogen cycle dominates in most cats.
D. All of the above are true
C. Telogen cycle dominates in most cats.
| *dominates in dogs.
82
Look at slide 33/2
.
83
What would you expect to see if you have an abnormal hormonal influence on the hair cycle?(Slide 34/2 KNOW)
By lateral symmetrical alopecia.
84
Market slides 35-40/2
.
85
Define vomiting.
Forcible ejection of gastric and occasionally proximal small intestinal contents through the mouth = emesis.
86
Define regurgitation.
Passive, retrograde movement of ingested material, usually before it has reached the stomach.
87
List if it is regurgitation or vomiting:
1. Doesn't typically have prodromal nausea.
2. Has forceful abdominal contractions.
3. May find bile.
4. May see distention of cervical esophagus.
1. Regurgitation
2. Vomiting
3. Vomiting
4. Regurgitation
88
What will you see with prodromal nausea?
Salivation, licking of lips, pacing, anxious expression.
89
What is responsible for controlling vomiting? (Part of the brain)
The Medulla (central nervous system)
90
What are the two centers that lead to vomiting?
The vomiting center (located in the reticular formation) and the chemoreceptor trigger zone (CTZ)(in the floor of the fourth ventricle).
91
Look at slide 40/3 for visual charts
.
92
What are the four things involved in the differential diagnosis scheme for vomiting?
– primary G.I. (peripheral direct): obstructive, inflammatory, infectious lesions of the stomach, small bowel or large bowel
– secondary G.I. (peripheral indirect): pancreatitis, renal disease, hepatic disease, diabetic ketoacidosis
– brain (central direct): anxiety, fear, pain, brain injury
– motion sickness (central indirect): motion sickness from the stimulator stimulation
93
What is considered to be rapid, inexpensive and the foundation upon which all future diagnostic procedures are selected?
History taking
94
What are the two general things in a full history?
– signalment and profile
| – owners primary complaint
95
What is involved in your signalman and profile?
Age, sex, free, diet, environment, vaccination status, medical history etc.
96
What complaints in the vomiting patient are secondary (less specific for gastrointestinal tract dysfunction)? (4)
– Fever
– dehydration
– anorexia/weight loss
– polyphagia/polydipsia/poluria
97
What are the five important things to look at for each clinical sign? (Slide 6/3)
Frequency, characteristics of vomitus/diarrhea, severity, acute versus chronic, screen other body systems.
98
Look at slide 10-11/3
.
99
A dog in the "praying position" is a sign of what?(Slide 12/3)
Abdominal pain
100
What are three things you look at for your physical examination?(slide13/3)
Temperature, pulse, respiration
101
What position is ideal to do an abdominal palpation on an animal? (Slide 17/3)
A standing animal
102
What is an abdominal auscultation most useful for detecting?
ileus - failure to detect borborygmus after 2-3 minutes
103
If you find the animal is systemically compromised with acute vomiting what should you do next?(Slide 18/3)
Further assessment to see if it's gastrointestinal tract or non-gastrointestinal tract.
104
What are the four tests you would run to see if the cause of vomiting is a non-gastrointestinal tract related?
Urinalysis, serum biochemistry, ultrasound, specific hormonal tests.
105
What would you look at the urinalysis to diagnose a non-gastrointestinal tract causes vomiting?
Serum biochemistry?
Ultrasound?
Specific hormonal tests?
Urinalysis:
– SG (the veranda renal disease, Cushing's syndrome)
– glucose for diabetes mellitus
Serum biochemistry:
– Liver enzymes (liver disease, Cushing's)
– liver function tests (e.g. bile acids etc.)
–urea and creatinine (renal disease)
– Amylase lipase (acute pancreatitis)
Ultrasound:
– visualize kidney, liver, pancreas, and adrenals.
Specific hormonal tests:
– ACTH stimulation test for Cushing's and Addison's
– T4 for hyperthyroidism (cats)
– gastrin levels
106
What is the initial laboratory work of a gastrointestinal tract case? (4)(slides 20 – 21/3)
– complete blood count (CBC)/blood smear
– fecal flotation
– fecal wet prep
– fecal smear
107
Look at slide 22/3 for treatment of acute vomiting serious systemically ill cases
.
108
What is the difference in pH between regurgitation and vomiting?
Regurgitation: >7
Vomiting: 8
109
Look at slide 35/3 for flowchart of regurgitation causes. (QUESTIONS MADE ON THAT SLIDE)
.
110
What are the systemic causes of vomiting? (7)
Diabetes ketoacidosis, renal failure, pancreatitis, hyperthyroidism, the biliary disease, hypoadrenocorticism, drug/toxin exposure.
111
What are the G.I. (stomach) causes of vomiting? (7)
Chronic gastritis, helicobacter, foreign body, gastric ulceration, gastric neoplasia, pyloric hypertrophy, motility disorder.
112
What are the G.I. (intestinal) causes of vomiting? (7)
Infectious bowel disease (IBD, parvovirus), neoplasia, foreign body, intussusception, extra intestinal obstruction, intestinal neoplasia, intestinal ulceration.
113
True or false: all species can vomit. (slide 42-43/3)
False
114
Look at slide 44 – 46/3
.A
115
What are the two types of cellular damage that can be found in acute kidney injury?
Sublethal and the lethal (necrosis, apoptosis)
116
What are the four processes that result in dysfunction in acute kidney injury?(Slide 7/4)
– Tubular obstruction
– back leakage of disrupted tubule
– vasoconstriction
– increased capillary permeability
117
What are the four stages of acute kidney injury?
Induction, extension, maintenance, and recovery.
118
What will you see during induction and extension stages of acute kidney injury?
Induction:
– insult occurs
– no clinical signs, but best time to intervene
– duration is variable
Extension:
– insults still present
– enough damage has occurred by clinical signs are now present
119
What will you see during maintenance and recovery stages of acute kidney injury?
Maintenance:
– causes gone now left with damage
– may go into recovery, CR, or worsen into anuric renal failure
– may last 1–3 weeks
Recovery:
– patient may slowly improve if damage to cells is sublethal
– during this time kidney function slowly improves
120
What are the two main causes of acute renal injury?
Perfusion inadequacies and toxins
121
Look at slide 11/4
.
122
Which of these is false referring to the pathophysiology of chronic renal failure?
A. Chronic renal failure leads to Damage and Loss
B. If the Number of nephron's falls below 1/3 Urine Concentrating Ability Becomes Impaired And Continues to 1/4 Azotemia Develops (CRF)
C. Further Progression of Damage and Azotemia Leads to Signs of uremic.
D. All of the above Are True
E. all of the above are false
D. All of the above Are True
123
Look at slide 14/4Has questions on it.
.
124
Why is chronic renal failure progressive?
Once chronic renal failure develops secondary processes are activated by contribute to renal damage.
125
What are the secondary processes that contribute to renal damage? (4)
– Systemic and the glomerular hypertension
– mineral imbalance
– proteinuria
– renal fibrosis
126
Look at slide 17/4
.
127
*KNOW THIS(slide 17/4)
| What are the five general signs you will see associated with chronic renal disease?
```
– PU/PD (nocturia)
– G.I. signs (vomiting, anorexia, weight loss, diarrhea, hyper celebration, constipation)
– depression/lethargy
– sudden onset blindness (rare)
– pathological fractures (rare)
```
128
What are the six things you would find on the clinical examination of an animal with chronic renal failure?
```
– dehydration
– poor body condition/underweight
– pale mucous membranes
– small kidneys
– hypertensive retinopathy
– loose teeth, deformable maxilla/mandible, fractures
```
129
What are your lab findings in chronic renal failure? (2)
– Azotemia (reduced GFR, increased catabolism, G.I. hemorrhage)
– inappropriately low urine specific gravity (unable to concentrate or dilute urine, cats SG (1.008 – 1.030), dogs SG (1.008 – 1.022))
130
What is the link between glomerular disease and tubulointerstitial disease?(Slide 21/4)
Proteinuria
131
What causes proteinuria?
Alterations in blood flow or inflammatory processes which may start in the tubule or glomerulus.
132
What is glomerulonephritis?
Group of conditions in which immune complexes are deposited in the glomeruli.
133
True or false: glomerulonephritis is more common in cats and dogs.
False, it's more common in dogs and cats
134
What is the most common cause of glomerulonephritis?(Slide 22/4)
Idiopathic (unknown cause)= 50%
135
Look at the slides 34 – 36/4
.
136
```
A dog with proteinuria due to low marry your disease is considered to have one of the following problems?
A. Renal failure
B. Renal disease
C. Azotemia
D. Uremia
```
B. Renal disease
137
```
A dog has isosthenuric urine (USG 1.008 – 1.012) without azotemia. What percentage of the kidneys damaged?
A. 35%
D. 50%
C. 66%
D. 75%
```
C. 66%
138
A dog has azotemia and inadequately concentrated urine (USG
A. Renal failure
B. Hyperadrenocorticism
C. Furosemide treatment
D. Phenobarbitone
139
Which statement is incorrect?
A. Normal water intake is 60-80 mL/kg/d
B. Normal urine production is 1-2 ml/kg/hr
C. Oliguria is urine production
D. Normal urine SG is 1.007-1.015
| *1.008-1.012
140
In cardiac disease we employ angiotensin-converting enzyme inhibitors. What effect will this have on the kidney?
A. Efferent vasodilator
B. Afferent vasodilator
C. increase ultra filtrate volume
D. Stimulate aldosterone and cause hypertension
A. Efferent vasodilator
141
```
When ACEi Rx is started we repeat blood tests 3 days later to monitor for which laboratory change?
A. Rise and sodium concentration
B. Rise in packed cell volume
C. Rise in creatinine
D. Rise in calcium
```
C. Rise in creatinine
142
What is not a feature of acute renal tubular injury?
A. renal tubular epithelial cells on sediment
B. Glucosuria
C. Proteinuria
D. High fractional excretion of sodium
E. Alkalosis
E. Alkalosis
143
```
A dog ingested ethylene glycol several hours ago. After a short period of ataxia noted by the owner, he has recovered. He is bright, alert and responsive. You run the blood tests and there is no azotemia. What phase of renal failure is this dog in?
A. Induction
B. Extension
C. Maintenance
D. Recovery
```
A. Induction
144
```
what is the most immediately life-threatening condition dogs and cats with oliguric renal failure?
A. Uremic encephalopathy
B. Hypertension
C. Hyperkalemia
D. Acid-base imbalance
E. Fluid overload
```
C. Hyperkalemia
145
```
A Six-Year-Old male neutered shih tzu brought to your clinic with the complaint of vomiting his food. The vomit had gained in the carpet yellow. Which statement is correct?
A. This is vomiting
B. This is regurgitation
C. This is expectoration
D. Unable to definitively confirm
```
A. This is vomiting
146
```
Adult presents to your clinic for vomiting. you perform laboratory tests and ascertained that he is offering from kidney failure. The afferent arm, stimulating the vomiting center is?
A. The video sympathetic trunk
B. The cortical open
C. Vestibular center the period
D. Chemo-emetic trigger zone
```
D. Chemo-emetic trigger zone
147
What are the three phases of wound healing?
Inflammation, proliferation, maturation
148
```
Which of the below represents the stage that repairs tissue?
A. Inflammation
B. Proliferation
C. Maturation
D. The stage is not listed
```
B. Proliferation
149
```
Which of the low represents the stage is known as the remodeling stage?
A. Inflammation
B. Proliferation
C. Maturation
D. The stage is not listed
```
C. Maturation
150
Define chronic wound.
Wounds that do not progress through the normal phases of wound healing. Usually do not progressed beyond the inflammatory phase.
151
When does the inflammatory stage happen during a wound?
| What are the three major players in the stage? (Think cells)
It happens immediately after wounding.
Platelets, neutrophils, monocytes
152
During the inflammatory phase, when will you see neutrophils and what are they responsible for?
You'll see them within 24 to 48 hours after wounding. They kill bacteria, break down Claude, phagocytosis, and release cytokines.
153
During the inflammatory phase, when will you see macrophages and what do they do?
You will see them 48 to 96 hours after wounding. The primary job is debridement and release cytokines to recruit other cells necessary for repair phase.
154
What days will you see the proliferation stage?
| What are their major players? (3)
You'll see this stage days 4 through 12.(A.k.a. constructive or repair phase)
major players: fibroblasts, endothelial cells, epithelial cells
155
What is angiogenesis, and why is it so important to the proliferation stage?
Is the process by which new capillaries are made and are present within four days.
It's important because it provides oxygen and nutrients to the wounded bed and lay foundation for granulation tissue.
156
What are responsible for recruiting fibroblasts? What do they synthesize, and what will they become? (Slide 10 PowerPoint)
Platelets and macrophages.
| They synthesize collagen, and become myofibroblasts.
157
How long does it take for granulation tissue to form? What will you find with granulation tissue?G
It takes 3 to 5 days. Within the granulation tissue you will find the capillary bed, fibroblasts, macrophages, collagen, fibronectin and hyaluronic acid.
158
What happens during the epithelialization portion of the proliferation stage?
Epithelial and endothelial cells proliferate. Cell migration along fibrin highways across the wound until contact inhibition occurs.
159
What happens during the maturation phase?
– Remodeling and strengthening.
– Thin, weak temporary matrix is reorganized and type III collagen is replaced by type I collagen.
– Collagen synthesis is inversely proportional to tension on the wound.
– Wound contraction is evident by days 5-9.
160
When is net collagen synthesis completed by?
| When is collagen maturation done by?
Synthesis is completed by 4-5 weeks.
| Maturation is done by 12-18 months.
161
What is the percent of normal wound strength by week one and week three?
By week one is 3% of what normal tissue strength would be.
| By week three it is at 30% of what normal tissue strength would be.
162
After how much time has passed would you reach 80% of the original tissue strength? Is this its maximum strength?
After three months it will achieve 80% and this is the maximum strength of it will achieve.
163
What are the four types of wounds management?
– Primary wound closure (first intention healing)
– Delayed primary closure
– Second intention healing
– Secondary closure (third intention healing)
164
How does primary wound closure work, and what is it used for?
Is appositional wound healing is achieved by using the wound edges together.
It is used in surgical wounds, clean wounds, and wounds with no tension.
165
What is the difference between a primary wound closure and the delayed primary wound closure?
The delay will take 3 to 5 days after the initial wounding but before the granulation tissue is present in the wound.
Indicated for mildly contaminated wounds that require cleaning, debridement and open wound management for a couple of days.
Decreases microbial contamination and improves tissue health for closure.
166
What is second intention healing?
| When would you use this?
Wounds not closed but left to heal by contraction and epithelialization.
Indicated for wounds that are highly contaminated and devitalized and will require open wound management for several days to weeks
*this type of healing can take a long time to happen.
167
What is secondary closure (third intention healing)?
Closing a wound 3-5 days after wounding by which time granulation tissue has formed in wound bed.
Wound is closed over the granulation tissue, although some debridement may be required.
*Granulation tissue is highly vascular and has exceptional antimicrobial properties
168
Look at slide 25-34/PP
.
169
What are the four things necessary for optimal intestinal healing?
– Good blood supply (shock).
– Accurate mucosal apposition (do not invert or evert the tissue edges).
– Minimal surgical trauma (never grasp intestine with thumb forceps!).
– Holding layer is submucosa!!!
170
How long does it take for the strength of a repair in the G.I. tract to be equal to that of normal intestine?
About 10 to 17 days
171
Why does the stomach heal faster than the small intestine and how long does it take?
Because the smooth muscle in the stomach is able to produce fibroblast, and it takes about 14 days.
172
Which animal heals faster cats or dogs?
Dogs.
173
Hypokalemia, non-regenerative anemia, acidosis and hyponatremia are all teachers of chronic kidney disease.
A. True
B. False
A. True
174
In chronic kidney disease, the patient suffers hypocalcemia due to low concentrations of calcitriol (vitamin D3) the biologically active form of vitamin D as the synthesis occurs in the kidney.
A. True
B. False
A. True
175
True or false: hypertension as a result of renal failure results in target organ damage (TOD). Target organs include, brain (seizures), heart (hypertrophic), kidney (progressive chronic kidney disease) and (detachment).
true
176
True or false:
When proteinuria is demonstrates by and you're in pre-teen creatinine ratio (UPCR), etiology the assumed to be glomerular in origin.
False
177
True or false:
In chronic kidney disease proteinuria (UPCR>0.4) can be severe(>3.5) and develops due to glomerular disease that eventually accompanies the syndrome.
False
178
```
In a PLN syndrome from glomerulonephritis which of the following clinical signs is typical?
A. Pulmonary edema
B. Diarrhea
C. Ascites
D. Hemorrhagic diathesis
```
C. Ascites
179
```
Which is not a feature of the nephrotic syndrome caused by PLN?
A. Hypoalbuminemia
B. Hypercholesterolemia
C. Proteinuria
D. Polyuria polydipsia
```
D. Polyuria polydipsia
180
```
A dog has hind limb ataxia and pollakiuria w/ a small bladder that is difficult to express. the neurolocalization is at which segment of the spinal cord?
A. Cervical
B. Cervicothoracic
C. Thoracolumbar
D. Sacral
```
C. Thoracolumbar
181
```
A dog has kind of lame paresthesia with incontinence, the bladder is large on palpation and easy to express. The neurolocalization is at which segment of the spine?
A. Cervical
B. Cervicothoracic
C. Thoracolumbar
D. Sacral
```
D. Sacral
