Flow Chart summary Flashcards

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1
Q

3 Key systems of Acid Base regulation?

A

Buffers
Resp
Renal

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2
Q

What is involved in Buffering Acid Base regulation?

A

HCO3- –> H2CO3

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3
Q

How does the Resp system control acid base?

A

Breathing off H+ from H2CO3

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4
Q

How doe the kidney work to control Acid base?

A

removing putting H from H2CO3 into ammonia and also reclaiming HCO3-

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5
Q

In HF what does the frank starling mechanism say happens?

A

Increase in preload = increase EDV = increase stretch :. increase contratility and release of ANP and ABP

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6
Q

How do Neurohumoral mechanisms operate in HF?

A

Nor adrenaline and RAAS

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7
Q

What does TGF-B and TNF-A do in HF?

A

Heart remodelling and Hypertrophy

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8
Q

What does ACE do to bradykinin?

A

Breaks down Bradykinin

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9
Q

What are the 3 stimuli for RAAS?

A

Decreased stretch in arterial circulation, decreased NaCl, decreased stretch in Afferent vessel to the kidney

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10
Q

Effects of AT2?

A

Increase blood volume by Aldosterone (Na), ADH (H2O)
Increase TPR by vasoconstriction
Long term effects include increase myocyte, Fibrosis in kidneys

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11
Q

3 classification of Acute renal Failure?

A

Prerenal, Intrarenal, Post renal

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12
Q

Causes of Hemodynamic abnormalities?

A

Myogenic reflex –> afferent dilation

Tubuloglomerula feedback –> RAAS

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13
Q

Out comes of tubular necrosis?

A

Tubular cells can not draw out Na
Junction disruption
Decreased GFR
Tubular cells slough off and block lumen –> woresening necrosis

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14
Q

Mutations in What predisposes to Alzheimers disease?

A

Change in APP processing

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15
Q

What are the outcomes of the amyloid angiopathy?

A

Friable vessels and likely to bleed

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16
Q

Genetic mutation involved in CF

A

Delta F508

17
Q

Disruption of what causes CF

A

Cystic Fibroisis Transmembrane Conductance Regulator

18
Q

What are the effects of distrupted CFTCR

A

Absent cAMP channel

19
Q

3 Organ specific outcomes of CF

A

Resp, Gastro, Sweat glands

20
Q

Likely outcomes of CF

A

Thick mucous in the airways –> infection

Leads to damage of pancreas A/B cells

21
Q

Chronic Inflammatory response is mediated through three pathways name them:

A

Macrophage activation and recruitment
Activation of lung Epithelium
Small airway inflammation

22
Q

What results from neutrophil release of IL-8 and TNF-A

A

Increase proteinase activity leading to destruction of elastin and irreversible damage.

23
Q

Result of small airway inflammation

A

Chronic bronchitis through goblet cell hyperplasia, SMC proliferation and resultant airway narrowing

24
Q

What does Pneumonia cause 2 main things

A

Intraalveolar exudate and inflmmation/ infection develops

25
Q

Common Signs of Crohns disease:

A
Fistulas
Diarrhoea
Lower right quadrant pain
Malnutrition
Inflammation
26
Q

RF’s for Crohns disease

A

Smoking
NSAIDS
INfection
NOD2

27
Q

How does Crohns disease develop

A

Dysfunctional Intestinal epithelium reacts inappropriately to Antigens to form a chronic inflammatory responce

28
Q

2 pathways to cirrhosis

A

Structural and or Functional

29
Q

What is involved in the structural pathway of cirrhosis

A

Fibrosis replaces hepatocytes leading to regenerative nodules which disrupt normal architecture.

30
Q

Outcomes of cirrhosis

A

Ascites from portal hypertension
Decreased Albumin
Bleeding through decreased vitamin K dependant clotting factors
Decreased gluconeogneosis

31
Q

4 Types of bleeds into parenchyma

A

Epidural
Subdural
Subarachnoid
Intracranial

32
Q

Epidural bleed Key points and outcome

A

Likely to herniate, commonly due to fracture

33
Q

Subdural bleed Key points and outcome

A

Rupture of bridging veins, often in elderly patients

34
Q

Subarachnoid Key points and outcome

A

Sudden rupture of a major vessel which can be either non-traumatic due to aneurysm or traumatic brain injury
WORST HEAD ACHE EVER

35
Q

Intracranial bleed Key points and outcome

A

Bleed into parynchema which will elicit mass effect when the bleed becomes big enough.