Okay, let's tackle this question. The user provided a question about congenital adrenal hyperplasia in a female child presenting with hypertension and androgenization. The correct answer is missing, so I need to figure out which enzyme deficiency causes these symptoms.

First, I remember that congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders affecting the adrenal cortex. The most common form is 21-hydroxylase deficiency. But the question mentions hypertension and androgenization. Let's think about the different enzyme deficiencies.

21-hydroxylase deficiency leads to accumulation of 17-hydroxyprogesterone, which leads to overproduction of androgens. In females, this can cause virilization. However, 21-hydroxylase deficiency typically causes salt-wasting or simple virilizing forms, but not usually hypertension. Hypertension is more commonly associated with 11β-hydroxylase or 17α-hydroxylase deficiencies because they lead to increased mineralocorticoid activity.

11β-hydroxylase deficiency blocks the conversion of 11-deoxycorticosterone to cortisol. This causes accumulation of 11-deoxycorticosterone, which has mineralocorticoid activity, leading to hypertension. Also, the deficiency leads to increased ACTH due to low cortisol, which stimulates the adrenal to produce more steroids, including androgens. So in females, this would cause virilization. That fits the symptoms given in the question: hypertension and androgenization.

17α-hydroxylase deficiency would block the production of both cortisol and sex steroids. The lack of cortisol would increase ACTH, leading to overproduction of mineralocorticoids (like deoxycorticosterone), causing hypertension. However, without 17α-hydroxylase, the pathway to androgens is blocked, so there wouldn't be androgenization. So this doesn't fit the question's scenario.

20,22-Desmolase deficiency is part of the 3β-hydroxysteroid dehydrogenase deficiency, which affects both glucocorticoid and mineralocorticoid synthesis. This usually leads to salt-wasting and ambiguous genitalia in females, but not hypertension.

So the correct answer here should be 11β-hydroxylase deficiency. The question mentions hypertension and androgenization in a female, which aligns with 11β-hydroxylase deficiency leading to mineralocorticoid excess and increased androgen production due to ACTH stimulation.

**Core Concept**
This question tests understanding of **congenital adrenal hyperplasia (CAH)** subtypes, specifically enzyme deficiencies affecting steroidogenesis. **11β-hydroxylase deficiency** is characterized by **hypertension** (due to mineralocorticoid excess) and **androgen excess** (virilization), while other enzyme deficiencies have distinct clinical profiles.

**Why the Correct Answer is Right**
**11β-hydroxylase deficiency** blocks cortisol synthesis from 11-deoxycortisol, leading to **accumulation of 11-deoxycorticosterone**, a potent mineralocorticoid. This causes **hypertension, hypokalemia, and metabolic alkalosis**. Concurrently, elevated ACT

✓ Correct Answer: B. C-11 hydroxylase