ascarbs

34 cards·by ascarbs

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Allopurinol

Gout XO blocks ua

Aminoglutethimide

Cushings Cholesterol Des Inh m g s

Exenatide

Diabetes GLP-1 ag promote I release ink gluc < appetite

Fludrocortisone

Add MinC res Aldosterone levels

Fluticasone

COPD GR Inh pro inflam, anti inflam

Indaxaterol

COPD PDE4 Bronch

Metformin

Diabetes Mito comp AMPK act < hepatic GNG

Metyrapone

Cushings C11B hydro Inh min and glu pathway

Pioglitazone

Diabetes PPARy ag < hep glu prod. promote > FA + G met

Salbutamol

COPD SABA Bronch

Titotropium Bromide

COPD Musc r M1 M3 Bronch and Inh muc secretion

Colchicine

Gout tubulin Disrupts mitotic spindle div

Trilostane

Cushings 3B-hydrosteroid dehydrogenase Restores aldosterone

Ipratropium Bromide

COPD Musc r M1 M3 Bronch and Inh muc secretion

Define what COPD is

Lung disease, causes airflow obstr not fully reversible, progressive, associated with inflam

Highlight key characteristics of COPD

Neutrophil migration, No AHR, No steroid response

COPD- what happens to FEV1, PEFR

both reduced, progressive airway obstruction

COPD- what happens to TLC

TLC increased, destruction of alveoli= increased lung vol

COPD- what happens to gaseous exchange

Poor gaseous exchange; high PaCO2 and low PaO2

What happens when smoke activates epi cells and alveolar macrophages- mediators released leading to disease progression- TGF-B

TGF-B multifunctional cytokine responsible for increased deposition of extracellular matrix in airwaves, and submucosal collagen expression

What happens when smoke activates epi cells and alveolar macrophages- mediators releasedleading to disease progression- CD8

hallmark feature > no of CD8 cells in airways lymph act= altered presentation of self antigensby cig smoke

What happens when smoke activates epi cells and alveolar macrophages- mediators released leading to disease progression- neutrophil

Neutrophilic inflammation predominates in airway wall + lumen. hypox can influence neut func impaired kill pathogenic ba, release proteases

What happens when smoke activates epi cells and alveolar macrophages- mediators released leading to disease progression-neutrophils lungs

Smoking attracts neut to lungs + there is an additional accu of neut, bc the abnormal antitrypsin polymerizes, acts as chemo attractant to n

alpha1 antitrypsin deficiency and COPD

Emphy=severe alpha1-antitrypsin deficiency- smoke. because of a deficient antiprotease protection against neut elastase release in the lung.

Explain why glucocorticoids are ineffective in COPD- pt 1

HDAC2- critical component in chain of react- enables corticos to < inflam, however HDAC2 subst < in lung tissue with COPD.

Explain why glucocorticoids are ineffective in COPD- pt 2

S-nitrosylation causes HDAC2 dysfunc + leads to CS insensitivity in alv macro of lungs with COPD

One novel approach for treating COPD

tmnt w/ sulforaphane restores HDAC2 activity and CS sensitivity by activating the Nrf pathway.

Name 3 drugs used in the clinical management of COPD. Why and MOA- 1

Salbutamol- B2 r ag- > cAMP, < Ach-relaxation of airways mimicking sym nervous sys.

Name 3 drugs used in the clinical management of COPD. Why and MOA- 2

Ipratropium Bromide- M3 r ant < bronchoconstriction- Inh PS nervous sys.

Name 3 drugs used in the clinical management of COPD. Why and MOA-3

Theophylline- PDE-4 inh prevent cAMP breakdown increased relax of airways- Theo also inh PI3 k leading to > HDAC2 + restoration steroid effi

What is Diabetes Mellitus

syndrome of chronic hyperg due to insulin deficiency/resistance symptoms. Usually irreversible.

Type 1 Diabetes

auto-immune disease (loss of I secreting b cells), treated with I.

Type 2 Diabetes

loss of ability to respond to I (I resistance). HyperI secretion but still inadequate torestore G homeostasis.

Type 1 Diabetes aetiology

Autoantibodies (I, GAD, IA-2, ZnT8) appear long pefore diabetes. Immune mediated islet cell destruction (a T cell dependent process)