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Pathophysiology > General: Topic 12-20 > Flashcards

General: Topic 12-20 Flashcards

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1
Q

What is the pH of arterial blood?

A

7.4

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2
Q

What is the pH of venous blood?

A

7.37

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3
Q

Which buffer system provides 90% of the buffer capacity?

A

H2CO3 buffer system

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4
Q

What can happen to bones during long term EC acidosis?

A

Mg2+, Ca2+, Na+, K+ are mobilised from the bone (exchanges with H+)

—> Long term demineralisation = Osteomalacia!

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5
Q

What are the three phases of pH restoration, and how long is the duration of the effect?

A
  1. Buffering period - Effect is prompt and short
  2. Fast organic compensation - 12-24 hours
  3. Slow organic compensation - up to 5 days
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6
Q

Which pH regulation is faster out of respiratory and renal regulation?

A

Respiratory regulation

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7
Q

How does the pH regulation of the lungs work?

A
  1. Fast regulation

2. Can only excrete acid (expiration of CO2)

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8
Q

How does the pH regulation of the kidneys work?

A
  1. Renal regulation is slower than respiratory

2. The kidneys can excrete BOTH acids and bases!

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9
Q

What are the two major changes / shifts during metabolic acidosis?

A

HCO3- decreases

pH decreases

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10
Q

What are the two major changes / shifts during respiratory acidosis?

A

pCO2 increases

pH decreases

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11
Q

What are the two major changes / shifts during metabolic alkalosis?

A

HCO3- increases

pH increases

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12
Q

What are the two major changes / shifts during respiratory alkalosis?

A

pCO2 decreases

pH increases

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13
Q

What is the main characteristic decrease (except for pH) in metabolic acidosis?

A

HCO3- (< 21 mmol/l)

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14
Q

What is the main characteristic decrease (except for pH) in respiratory acidosis?

A

pCO2- increase (>40 Hgmm)

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15
Q

Name three endogenous reasons for metabolic acidosis

A
  1. Ketoacidosis
  2. Lactate acidosis
  3. Hypoxia
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16
Q

Name three exogenous reasons for metabolic acidosis

A
  1. Overfeeding of acidic feeds (containing e.g. elevated butyrate content in silage)
  2. Overdosing on acidifying infusions
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17
Q

Name the four main reasons why metabolic acid occurs

A
  1. Endogenous: Acid formation increase
  2. Exogenous: Acid intake increase
  3. Acid excretion decrease
  4. Alkaline loss increases
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18
Q

How does alkaline loss from the body occur?

A
  1. Diarrhoea

2. Prolonged hyper-salivation

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19
Q

How does acid excretion from the body decrease?

A
  1. Renal failure

2. Hyperkalaemia (H+ / K+ pump!)

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20
Q

What are the two forms of respiratory acidosis?

A
  1. Central form

2. Peripheral form

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21
Q

How / why does the central form of respiratory acidosis occur?

A

Main = Caused by damage of CNS of peripheral nerves

  1. Hypofunction of resp. Centre as a result of anaesthesia or trauma
  2. Disorders of respiratory muscle innervations
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22
Q

How / why does the peripheral form of respiratory acidosis occur?

A

Main = Decreased pulmonary function

  1. Mechanical causes such as obfuscation, thoracic trauma, or chest deformity
  2. Chest or lung diseases; e.g. oedema, inflammation, PTX, pleuritic, smoke poisoning
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23
Q

What are the two main causes for metabolic alkalosis?

A
  1. H+ loss increase

2. Alkali overload

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24
Q

What leads to the increased H+ loss during metabolic alkalosis?

A
  1. Vomiting (HCl loss)
  2. Abomasal displacement
  3. Hypokalaemia
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25
What leads to alkali overload, which again leads to metabolic alkalosis?
1. Primary + Sec. Hyperaldosteronism (can lead to an inc. alkaline and NA+ retention) 2. Increase in exogenous base intake (E.g. urea)
26
What are the two main forms of respiratory alkalosis?
1. Central hyperventilation | 2. Peripheral hyperventilation
27
What is the main cause of respiratory alkalosis?
Primary and secondary hyperfunction of the respiratory centre
28
What are some other conditions that can occur simultaneously with central hyperventilation (resp. alk.)
1. Fever 2. Hyperthermia 3. Stress 4. Trauma to the head 5. Analeptics effect 6. Encephalitis 7. Meningitis
29
What are some other conditions that can occur simultaneously with peripheral hyperventilation (resp. alk.)
1. Hypoxaemia 2. Hypercapnia 3. Pneumonia 4. (At the beginning of) Lung oedema
30
What does physical thermoregulation regulate?
Heat loss
31
What does chemical thermoregulation regulate?
Heat production
32
What does physical thermoregulation consist of?
1. Conduction 2. Convection 3. Evaporation 4. Radiation
33
What does chemical thermoregulation consist of?
1. Shivering (O2 needed) | 2. Non-shivevring
34
“Core” temperature is considered to the the temperature of which main organs?
1. Brain 2. Thorax 3. Abdomen
35
Name one result of local heat exposure
Burns (combustion)
36
What is the definition of general heat exposure?
An unregulated rise in body temperature, which has no pathogenic or hypothalamic origin
37
Which condition(s) develop when there is a larger heat gain than heat loss?
Hyperthermia or heat stroke
38
What is the physical reaction to hyperthermia?
1. Hyperventilation 2. Tachycardia 3. Vasodilation 4. Perspiration 5. Shock 6. Decrease in the function of the CNA and muscles
39
In which species is malignant hyperthermia most common?
In pigs (and humans)
40
What can be seen in a case of malignant hyperthermia?
Elevated IC Ca2+
41
What can trigger malignant hyperthermia?
1. Halothane | 2. Muscle relaxants
42
True or false: Heat stroke and malignant hyperthermia are the same thing
False
43
Name some exogenous causes of hyperthermia
1. Toxins (Hexachlorophene, mycotoxins, organic phosphates, etc.) 2. Opioids 3. Muscle tremor-inducing (I.e. tremorgenic) drugs 4. Environment (temperature, humidity)
44
Name some endogenous causes for hyperthermia
1. Seizures (Status epilepticus) 2. Eclampsia (dog milk fever) 3. Physical activity (mainly carnivores and equines) 4. Anhydria in equines 5. Lack of condition / acclimatisation 6. Previous overheating episodes
45
Name the four different types of hyperthermia
1. Heat cramps 2. Heat exhaustion 3. Heat prostration 4. Heat stroke
46
What are heat cramps, and what are they marked by?
The most common heat-induced illness in humans (rarely in animals). Marked by muscle cramps, Na+ depletion, and extreme dehydration
47
What is heat exhaustion, and what is it marked by?
A more advanced form of heat induces illness. Inability to perform work due to lethargy from extreme heat conditions
48
What marks heat prostration?
Marked by headache, vomiting, hypotension, and tachycardia
49
What is a heat stroke, and what is the general description?
The most severe form of heat induced illness in humans Marked by; Circulation insufficiency, CNS dysfunction, and the breakdown of enzymatic and cellular functions
50
What happens in the circulation during a heat stroke?
Circulatory collapse 1. Inc. heart rate 2. Vasodilation 3. Hypovolaemia
51
What type (speed) of condition is a heat stroke?
Acute (and life threatening) / Emergency
52
What is the global damage of a heat stroke?
1. Increase in liver enzymes 2. Azotaemia (High N in blood) 3. Acute renal failure —> Oliguria 4. Loss of GI integrity (septic shock possible)
53
Name the most important pathophysiological processes of a heat stroke
1. Circulatory collapse 2. Global damage to endothelium 3. Metabolic acidosis (inc. Lactate) or resp. Alkalosis 4. Hyper-Na+, -K+, -Ca2+, and hypophosphataemia 5. Coagulopathies / DIC 6. Neurological disturbances
54
Which animals can be affected by malignant hyperthermia?
PIgs, humans, horses, dogs
55
What is a local effect of hypothermia?
Frostbite
56
Where can local effects of hypothermia most often be seen?
Mucous membranes and skin
57
What is the effect of vasoconstriction during hypothermia?
1. Tissue O2 drops, Tissue CO2 increases 2. Local defences decrease in strength 3. Frostbite develop
58
What marks general hypothermia?
Decreased core temperature or blood temperature, which causes a malfunction of the organs
59
What are the main affected areas during general hypothermia?
1. Blood and circulation 2. Respiratory apparatus 3. Liver, kidney 4. Muscles (react with shivering thermogenesis) 5. Endocrine glands (react with non-shivering thermogenesis)
60
What are the four characteristics of hibernation?
1. Sleep 2. Muscle relaxation 3. A fall in the metabolic rate 4. Lowered body temperature
61
Which type of drug can induce a hibernation-like state?
Tranquilizers
62
What is the definition of a fever?
A regulated rise in body temperature that has an endogenous origin, and is independent from the environmental temperature
63
What are the three sources of a fever?
1. Endogenous source 2. Exogenous source 3. Drugs
64
What are the endogenous causes of a fever?
Endogenous Pyrogens / Granulocyte pyrogens (TNF-alpha, IL-6)
65
What are the exogenous causes of a fever?
Exogenous pyrogens (Microorganisms and their toxins; LPS)
66
What does pyrogens do?
They elicit a response in Interleukin-1’s (WBC, astrocytes) which decreases the sensitivity of the heat regulating centre by inducing PGE2 production, which increases the “temperature set point” of the hypothalamus
67
What does FUO stand for?
Fever of Undetermined Origin
68
What are the sources of FUO?
``` 35% Infections (not only bacterial) 20% Tumours 15% Autoimmune diseases 15% Other factors (E.g. inflammation or drugs) 15% Unknown ```
69
What are the characteristic physiological effects of a fever?
1. Increased metabolic demand and O2 consumption 2. Vasodilation 3. Discomfort
70
Name at least 5 stressors
1. Trauma 2. Fear 3. Pain 4. Warmth / cold 5. Norepinephrine 6. Glucose decrease 7. Immobilisation 8. Deteriorating disease 9. Surgical treatment 10. Can be non-specific
71
What is the effect of a stressor that lasts for 1-2 minutes?
There is an activated sympathicotonia, which releases catecholamines via the adrenal medulla
72
What is the ratio (%) of catecholamines released during stress?
80% Epinephrine | 20 % Norepinephrine
73
Which receptors are stimulated by catecholamine release?
1. Alpha receptors: Causes vasoconstriction (not in GT) 2. Beta-1: Causes in inc. heart rate + Inc. blood pressure 3. Beta-2: Causes vasodilation
74
What are the three mechanisms an organism can display during an environmental stressor?
1. Reaction: Fast (seconds / minutes) 2. Adaption: (Via nervous and endocrine systems) Slow (days / weeks) 3. Deformation: Very strong stimulus (over a long period of time)
75
What is the additional reactive pathway in the event of a long lasting stressor?
Brain cortex participation
76
What happens in the brain cortex participation pathway in the event of a long term stressor?
1. The hypothalamus releases CRF 2. CRF stimulate the hypophysis to release ACTH 3. ACTH reaches the adrenal cortex 4. The adrenal cortex releases glucocorticoids
77
What is CRF (released by the hypothalamus)?
Corticotropin-releasing factor
78
What is ACTH (released by the hypophysis)?
Adrenocorticotropin hormone
79
Where is ACTH released from?
The hypophysis
80
Where is Corticotropin-releasing hormone released from?
The hypothalamus
81
What is the reason for glucocorticoid and catecholamine production in the body?
Alarm reaction (stress) (fight or flight)
82
What can the physiological alarm reaction (fight or flight) reaction result in?
1. Exhaustion (death) | 2. Adaption (and following that, adaption disorders / diseases)
83
Which types of hormones are produced by the Zona glomerulosa of the adrenal cortex?
Mineralocorticoids
84
Where are mineralocorticoids produced?
In the Zona glomerulosa of the adrenal cortex
85
Which types of hormones are produced in the Zona fasciculata of the adrenal cortex?
Glucocorticoids
86
Where are glucocorticoids produced?
In the Zona fasciculata of the adrenal cortex
87
Which types of hormones are produced in the Zona reticular is of the adrenal cortex?
Androgens
88
Where are androgens produced?
In the Zona reticularis of the adrenal cortex
89
What are the physiological actions of cortisol?
1. Promotes GNG 2. Promotes breakdown of skeletal muscle protein 3. Enhances lipolysis 4. Suppresses the immune system 5. Anti-inflammatory effects 6. Breaks down bone matrix in high doses
90
What are the anti-inflammatory effects of cortisol?
1. Reduces the phagocytise action of WBC 2. Reduces fever 3. Suppresses allergic reactions
91
What is the effect of cortisol on blood cells and immunity?
1. Dec. production of Eosinophils and lymphocytes | 2. Suppresses lymphoid tissue —> T-cell and antibody production decrease = Immunity decrease
92
Name one example in which the use of cortisol could be lethal
In the case of diseases like e.g. tuberculosis | -> Lowers immune system; body cannot put up a fight
93
Name one example in which the use of cortisol is useful
During organ transplantation (reduces immunity = Reduces the likelihood of organ rejection)
94
Name some behavioural signs of adaptation disorders
1. Decreased production (milk, meat, eggs, wool) 2. Feather picking (birds) 3. Tail biting (pigs) 4. Chewing wood (horses) 5. Cannibalism
95
What are some symptoms of haemorrhagic diathesis?
1. Petechia 2. Ecchymosis 3. Haematoma 4. Hemothorax, hemoperitoneum, hemocardium
96
What is petechia?
A tiny spot of haemorrhage on the surface of the skin, organs, mucous-, or serous membranes
97
What is ecchymosis?
Diffuse bleeding into the subcutaneous tissue and skin
98
What is a haematoma?
Extravascular, circumscribed collection of blood in tissues
99
How can hemothorax, hemoperitoneum, and hemopericardium be defined?
As an accumulation of blood in serous body cavities
100
What is coagulopathy?
Disorders of coagulation mechanisms
101
What is Thrombocytopathy?
Platelet disorders
102
What is vasopathy?
Blood vessel disorders
103
Name the 4 types of haemostasis disorders
1. Coagulopathy 2. Vasopathy 3. Thrombocytopathy 4. Complex
104
What are some typical lab results in haemorrhagic disorders?
1. Prolonged coagulation time (CT), clotting time 2. Prolonged bleeding time 3. Changes in prothrombin time (PT), Activated Partial Thromboplastin Time (ATPP), and platelet count
105
What are the two main forms of coagulopathies?
1. Congenital (rare) | 2. Acquired (common)
106
What is the problem during a congenital coagulopathy?
There is a deficiency of a single coagulation factor (e.g. Factor VIII), causing a deficiency in the thromboplastin production
107
What are the characteristics of a congenital coagulopathy?
1. Increased clotting time 2. Increased bleeding time 3. PT and ATPP is normal or increased
108
In haematology, what does PT mean?
Prothrombin time
109
What does it mean when PT is increased in haematology?
There is an EXTRINSIC pathway dysfunction
110
What does APTT mean in haematology?
Activated partial thromboplastin time
111
What does it mean when APTT is increased?
That there is a problem with the INTRINSIC pathway
112
What does TT stand for in haematology?
Thrombin time
113
What does it mean when TT is increased?
That these is a problem with the COMMON pathway
114
What is Von Willebrand’s disease?
``` A combined coagulation and platelet disorder Factor VIII (8) is low, and thereby platelet adhesiveness is lowered ```
115
In which animal is Von Willebrand’s disease most often seen?
In dogs
116
What can be the cause of fibrinogen deficiency (4th phase)?
1. Severe hepatic damage 2. Severe cahexia 3. Increase of fibrinolytic compounds 4. Increased utilisation
117
What can be the result of fibrinogen deficiency?
1. Protein deficiency | 2. DIC
118
What does DIC stand for?
Disseminated Intravascular coagulopathy
119
Describe what happens during DIC
1. Blood clotting happens in many places throughout the body, and can block small capillaries 2. Clotting factors and platelets gets used up
120
What can be the cause of a prothrombin deficiency or a decreased prothrombin production?
1. Lack of thrombin production (3rd phase involved) 2. Impaired hepatic function 3. Vitamin K deficiency 4. Increased utilisation
121
Does these disorders cause minor or major bleeding? 1. Coagulopathy 2. Vasopathy 3. Thrombocytopathy
1. Major bleeding (ecchymosis, haematoma) 2. Minor (petechia) 3. Minor (petechia)

Pathophysiology (5 decks)

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